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Chronic musculoskeletal pain (CMP) is associated with an increased risk of cardiovascular disease (CVD). This study aimed to determine the factors associated with the intensity of CMP in patients with underlying CVD and to evaluate the efficacy of Ice Power Magnesium In Strong Cream in patients with muscle cramps. We investigated 396 patients with or without CMP who visited an outpatient cardiology clinic and analyzed the features of CMP and factors associated with pain intensity and specific types of CVD in study 1. We also analyzed 73 patients who had muscle cramps in the lower extremities in study 2 to evaluate the efficacy of Ice Power Magnesium In Strong Cream in reducing pain intensity. In study 1, multivariable linear regression analysis showed that older age (regression coefficient [B] = 0.66, 95% confidence interval [CI], 0.07-1.24), female sex (B = 1.18, 95% CI, 0.59-1.76), presence of hypertension (B = 0.69, 95% CI, 0.05-1.33), and use of calcium supplements (B = 1.27, 95% CI, 0.31-2.24) were significantly associated with a higher intensity of CMP. In study 2, the mean pain scores at baseline, week 2 and week 4 after treatment were 5.99 ± 2.12, 2.92 ± 2.63, and 1.90 ± 2.41, respectively, and the reductions were significant at both week 2 and week 4 after treatment (P < .05). Older age, female sex, hypertension, and use of calcium supplements were associated with an increased intensity of CMP. Ice Power Magnesium In Strong Cream was effective in reducing the pain intensity of muscle cramps in the lower extremities., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Hypertension is the leading preventable risk factor for cardiovascular disease and all-cause mortality worldwide. However, studies have shown increased risk of mortality from heart disease and stroke even within the normal blood pressure (BP) range, starting at BPs above 110-115/70-75 mm Hg. Nutraceuticals, such as vitamins and minerals, have been studied extensively for their efficacy in lowering BP and may be of benefit to the general, normotensive population in achieving optimal BP. Our study investigated the effects of six nutraceuticals (Vitamins: C, D, E; Minerals: Calcium, Magnesium, Potassium) on both systolic blood pressure (SBP) and diastolic blood pressure (DBP) in this population. We performed a systematic review and pairwise meta-analysis for all six supplements versus placebo. Calcium and magnesium achieved significant reductions in both SBP and DBP of -1.37/-1.63 mm Hg and -2.79/-1.56 mm Hg, respectively. Vitamin E and potassium only yielded significant reductions in SBP with values of -1.76 mm Hg and -2.10 mm Hg, respectively. Vitamins C and D were not found to significantly lower either SBP or DBP. Future studies should determine optimal dosage and treatment length for these supplements in the general, normotensive population.

Introduction: Lower-sodium oxybate (LXB) is a novel formulation that is approved by the US Food and Drug Administration (FDA) to treat cataplexy and excessive daytime sleepiness (EDS) in adult patients and children ≥7 years with narcolepsy. LXB contains 92% less sodium than sodium oxybate (SXB), which adds 550-1640 mg of sodium/day at usual doses of 3-9 g/day. The FDA has declared LXB to be clinically superior to SXB due to greater safety by reducing the chronic sodium load. Narcolepsy patients have high comorbidities for hypertension and cardiovascular disease conditions, which can be adversely affected by high sodium intake., Areas Covered: This drug review discusses narcolepsy, current and upcoming pharmacotherapy, and LXB chemistry, pharmacodynamics, pharmacokinetics, and metabolism. Published results from LXB's phase 1 studies, a phase 3 study, and two post-marketing studies are reviewed. Databases searched included PubMed, Google Scholar, Lexi-Comp, Scopus, Science, and Ovid., Expert Opinion: LXB is efficacious in treating daytime sleepiness and cataplexy in adults and children ≥7 years with narcolepsy. Using LXB instead of SXB formulations may benefit narcolepsy patients with cardiovascular comorbidities and hypertension, but long-term studies are needed to prove it.

Objective: The aim: The current study was designed for evaluation the effect of oral magnesium l-lactate supplementation on blood pressure and corrected QT interval in a sample of Iraqi women., Patients and Methods: Materials and methods: In this interventional prospective randomized trial, 58 female patients diagnosed with MetS according to the International Diabetic Federation (IDF) criteria and were randomly allocated to receive either placebo or magnesium l-lactate 84 mg, twice daily., Results: Results: O#ce blood pressure showed a signi$cant drop in systolic blood pressure (SBP) (P<0.05), non-significant decline in diastolic blood pressure (DBP), heart rate (HR), and pulse pressure (PP) (P>0.05), while ambulatory blood pressure monitoring (ABPM) recorded a signi$cant reduction in HR in patients on magnesium supplement. Also, there was a signi$cant decline in the SBP (P<0.05) and non-signi$cant decline in DBP and PP (P>0.05) in patients with masked hypertension on Mg supplement. The changes in corrected QT- interval had no signi$cant e"ect within Mg group (P>0.05)., Conclusion: Conclusions: From above results, one can conclude that oral Mg l-lactate supplement can improve, to a certain extent, blood pressure of women with MetS. Further studies in this aspect may be required.

Due to the versatility of its functions and participation in all types of metabolism, magnesium can be considered the main cation in the human organism. Equally important is the role of the main intracellular ion - potassium, which is a synergist of magnesium, especially with regard to the effect on cardiovascular system function. In Russia, there is insufficient consumption of magnesium and potassium by the population. The purpose of the work was to assess the role of magnesium and potassium in ensuring public health. Material and methods . Literature search was carried out using PubMed, Google Scholar, ResearchGate, RISC systems mainly over the past 10 years, with the exception of works of fundamental importance, according to the keywords "magnesium", "bioavailability", "potassium", "efficiency". Results . Chronic hypomagnesemia and hypokalemia are involved in the pathogenesis of various metabolic disorders (metabolic syndrome, insulin resistance and type 2 diabetes mellitus, hypertension, hyperlipidemia and sluggish inflammation). Magnesium deficiency increases the risk of cardiovascular (arrhythmia, hypertension, heart failure), neurological diseases (stroke) and depression, as well as diseases of the respiratory system (bronchial asthma, chronic obstructive pulmonary disease). Potassium deficiency is also associated with pathology of the cardiovascular system. Adequate intake of magnesium and potassium with food and/or dietary supplements prevents the development of chronic metabolic complications. Various magnesium compounds used to correct its deficiency, have different bioavailability. Conclusion . The expediency of compensating for magnesium and potassium deficiency in nutrition has been proven both for preventive purposes in a healthy person and as part of diet therapy in a patient. Enrichment of the diet with magnesium and potassium is a reliable non-drug, economical and safe prevention of chronic deficiency and associated metabolic disorders., Competing Interests: The authors declare no overt and potential conflict of interest related to the publication of this article., (Copyright© GEOTAR-Media Publishing Group.)

Trials and meta-analyses of oral magnesium for hypertension show promising but conflicting results. An inclusive collection of 49 oral magnesium for blood pressure (BP) trials were categorized into four groups: (1) Untreated Hypertensives; (2) Uncontrolled Hypertensives; (3) Controlled Hypertensives; (4) Normotensive subjects. Each group was tabulated by ascending magnesium dose. Studies reporting statistically significant ( p < 0.05) decreases in both systolic BP (SBP) and diastolic BP (DBP) from both baseline and placebo (if reported) were labeled "Decrease"; all others were deemed "No Change." Results: Studies of Untreated Hypertensives (20 studies) showed BP "Decrease" only when Mg dose was >600 mg/day; <50% of the studies at 120-486 mg Mg/day showed SBP or DBP decreases but not both while others at this Mg dosage showed no change in either BP measure. In contrast, all magnesium doses (240-607 mg/day) showed "Decrease" in 10 studies on Uncontrolled Hypertensives. Controlled Hypertensives, Normotensives and "magnesium-replete" studies showed "No Change" even at high magnesium doses (>600 mg/day). Where magnesium did not lower BP, other cardiovascular risk factors showed improvement. Conclusion: Controlled Hypertensives and Normotensives do not show a BP-lowering effect with oral Mg therapy, but oral magnesium (≥240 mg/day) safely lowers BP in Uncontrolled Hypertensive patients taking antihypertensive medications, while >600 mg/day magnesium is required to safely lower BP in Untreated Hypertensives; <600 mg/day for non-medicated hypertensives may not lower both SBP and DBP but may safely achieve other risk factor improvements without antihypertensive medication side effects.

: High-normal blood pressure (BP) is associated with an increased risk of cardiovascular disease, however the cost-benefit ratio of the use of antihypertensive treatment in these patients is not yet clear. Some dietary components and natural products seems to be able to significantly lower BP without significant side effects. The aim of this position document is to highlight which of these products have the most clinically significant antihypertensive action and wheter they could be suggested to patients with high-normal BP. Among foods, beetroot juice has the most covincing evidence of antihypertensive effect. Antioxidant-rich beverages (teas, coffee) could be considered. Among nutrients, magnesium, potassium and vitamin C supplements could improve BP. Among nonnutrient-nutraceuticals, soy isoflavones could be suggested in perimenopausal women, resveratrol in insulin-resistant patients, melatonin in study participants with night hypertension. In any case, the nutracutical approach has never to substitute the drug treatment, when needed.

Background: Epidemiological studies demonstrate an inverse association between serum magnesium and incidence of cardiovascular disease. Diuretics commonly cause hypomagneseamia., Method: We evaluated effects of magnesium supplementation on blood pressure (BP) and vascular function in thiazide-treated hypertensive women in a randomized, double-blind, clinical trial. Hypertensive women (40-65 years) on hydrochlorothiazide and mean 24-h BP at least 130/80 mmHg were divided into placebo and supplementation (magnesium chelate 600 mg/day) groups. Patients were evaluated for nutritional and biochemical parameters, office and ambulatory blood pressure monitoring, brachial flow-mediated dilatation (FMD), peripheral arterial tonometry, assessment of carotid intima-media thickness, central hemodynamic parameters and pulse wave velocity at inclusion and after 6-month follow-up., Results: The magnesium group had a significant reduction in SBP (144 ± 17 vs. 134 ± 14 mmHg, P = 0.036) and DBP (88 ± 9 vs. 81 ± 8 mmHg, P = 0.005) at 6 months, without effect on plasma glucose, lipids, or arterial stiffness parameters. The placebo group showed a significant increase in carotid intima-media thickness (0.78 ± 0.13 vs. 0.89 ± 0.14 mm, P = 0.033) without change in the magnesium group (0.79 ± 0.16 vs. 0.79 ± 0.19 mm, P = 0.716) after 6 months. The magnesium group demonstrated a significant increase in variation of FMD vs. the placebo group (+3.7 ± 2.1 vs. 2.4 ± 1.2%, P = 0.015). There was a significant correlation between the intracellular magnesium variation and FMD (r = 0.44, P = 0.011)., Conclusion: Magnesium supplementation was associated with better BP control, improved endothelial function and amelioration of subclinical atherosclerosis in these thiazide-treated hypertensive women.

Previously we found that hypertension potentiates the risk the cataractogenesis. In the present study, we investigated the protective effects of magnesium taurate (MgT) on hypertension and associated lenticular damages against cadmium chloride (CdCl 2 )-induced hypertensive animals. Male Sprague-Dawley albino rats (150-180g) were assigned to five experimental groups (n=6). Among the five groups, normal group received 0.3% carboxymethyl cellulose (10ml/kg/day, p.o.). Hypertension control group received CdCl 2 (0.5mg/kg/day, i.p.). Tests and standard groups received MgT (3 and 6mg/kg/day, p.o.) and amlodipine (3mg/kg/day, p.o.) concurrently with CdCl 2 respectively , for six consecutive weeks. Blood pressure, heart rate, and eyes were examined biweekly, and pathophysiological parameters in serum and eye lenses were evaluated after six weeks of the experimental protocol. The chronic administration of MgT concurrently with CdCl 2 significantly restored the blood pressure, serum and lens antioxidants (CAT, SOD, GPx, and GSH), MDA level, and ions (Na + , K + , and Ca 2+ ). Additionally, MgT treatment led to significant increase in the lens proteins (total and soluble), Ca 2+ ATPase, and Na + K + ATPase activity as compared to hypertension control group. Ophthalmoscope observations indicated that MgT treatments delayed the progression of cataract against the hypertensive state. The study shows that MgT prevents the progression of cataractogenesis via restoration of blood pressure, lenticular oxidative damages, and lens ATPase functions in the hypertensive state. The results suggest that MgT supplement may play a beneficial role to manage hypertension and associated cataractogenesis., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)

Hypertension is the most important, modifiable risk factor for cardiovascular disease and mortality. High salt intake may predispose children to develop hypertension later. A modest reduction in population salt intake worldwide would result in a major improvement in public health. Regarding smoking as another risk factor, there are various strategies that can be used to promote smoking cessation. Physicians are in an excellent position to help their patients stop smoking. Targeted weight loss interventions in population subgroups might be more effective for the prevention of hypertension than a general-population approach. A diet rich in high-potassium fruit and vegetables is strongly recommended. Fresh products are best; normal potassium content is reduced when foods are canned or frozen. Calcium supplementation reduces blood pressure in hypertensive individuals during chronic nitric oxide synthase inhibition and high calcium diet enhances vasorelaxation in nitric oxide-deficient hypertension. Magnesium should be considered by anyone seeking to prevent or treat high blood pressure. The foundation for a healthy blood pressure consists of a healthy diet, adequate exercise, stress reduction, and sufficient amounts of potassium and magnesium, but further investigations are required before making definitive therapeutic recommendations on magnesium use. Alcohol usage is a more frequent contributor to hypertension than is generally appreciated. For hypertensive patients in whom stress appears to be an important issue, stress management should be considered as an intervention. Individualized cognitive behavioral interventions are more likely to be effective than single-component interventions.

Introduction: European Society of Hypertension (ESH/ESC) and Polish Society of Hypertension (PTNT) guidelines do not recommend magnesium supplementation as an adjunctive therapy of patients with arterial hypertension. Nevertheless, Polish Institute of Food and Nutrition suggests increased supplementation of magnesium ions among hypertensive patients in everyday diet., Aim: The aim of the study was to assess a frequency of using magnesium supplements by hypertensive patients including demographic and clinical characteristics of the study group., Metodology: From October 2015 to January 2016 data of 309 hypertensive patients from Outpatient Clinic were collected and analyzed. We assessed: demographic and medical therapy data, results of office blood pressure and heart rate measurements., Results: We collected data of 309 patients aged between 19 and 84 (mean age 54.9±15.2 years) who were diagnosed with hypertension (HA). Mean time from diagnosis of HA was 12.8±9.9 years. The study group was represented in majority by subjects with secondary school level (40.8%) and university education (31.7%), retried (38.5%) or white-collars (26.9%). The proportion of patients using magnesium supplementation was 47.9% in the study group. Women more common than men were using magnesium supplements (68.2%, p=0.0001). Subjects preferred organic forms of magnesium supplements (85.1%) rather than inorganic (11.5%) or chelats (3.4%). There was no significant differences in SBP (142 vs 140 mmHg; p=0.93), DBP (80 vs 82 mmHg; p=0.42) and HR (71.5 vs 70.0 per min.; p=0.21) in group with and without magnesium supplementation. Pharmacological treatment and the proportion of patients that reach BP target (BP< 140/90 mmHg) were comparable in subgroup’s analysis., Conclusions: Nearly half of hypertensive patients, especially women, use magnesium supplements regularly. Organic forms are preferable. Supplemental doses of magnesium ions did not associate with SBP, DBP and HR values and reaching BP target in hypertensive patients.

The aim of this study was to determine the relationship between serum magnesium (Mg) concentrations in middle-aged and older men, and the occurrence of selected metabolic and hormonal disorders. The study involved a total of 313 men aged 50-75 years, and who underwent standard anthropometric measurements. Also determined were blood serum Mg, lipid parameters - total cholesterol (TCh), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglyceride (TG) and carbohydrate metabolism parameters - glucose, insulin (I). In men with a normal total testosterone (TT) concentration, serum Mg was significantly higher compared to patients with a total testosterone deficiency. The subjects with metabolic syndrome had lower serum Mg compared to patients without metabolic syndrome. Serum Mg concentration in type 2 diabetes mellitus was lower compared to men without diabetes. In patients with arterial hypertension, serum Mg concentration was lower than in patients without hypertension. Statistically significant negative correlations were found for the relationships between Mg concentration and body mass index, waist-to-hip ratio, abdominal circumference, arterial blood pressure. Statistically significant, positive correlations were found for the relationships between Mg concentration and TT, TCh, LDL concentrations. The lower serum Mg level may be conducive to the development of total testosterone deficiency, arterial hypertension, diabetes, and therefore metabolic syndrome.

This study investigated the effect of magnesium on the vascular reactivity of conduit and resistance arteries in a nitric oxide synthase inhibition-induced hypertension model. The aorta and third-order branches of the mesenteric artery were dissected from normotensive control and hypertensive rats, and their constriction and dilation responses in physiological saline solution containing normal (1.2 mM) or high (4.8 mM) magnesium concentrations were examined. The responses of the vessels were evaluated using potassium chloride (KCl) and phenylephrine (Phe), acetylcholine (ACh) and sodium nitroprusside. The Phe-induced constriction response of the aortic rings increased, whereas the ACh-induced dilation response decreased, in the hypertensive group compared to controls, in the presence of a normal magnesium concentration. High magnesium did not alter these responses in either group. Both the KCl- and Phe-induced constriction responses of the mesenteric arteries increased, and the ACh-induced dilation response decreased in the hypertensive group compared to controls, in the presence of a normal magnesium concentration. High magnesium significantly decreased the KCl and Phe-induced constriction and increased the ACh-induced dilation response of the mesenteric arteries in the hypertensive group, while it did not alter these responses in controls. This study suggests that high magnesium improves vascular reactivity of resistance-, but not conduit-type arteries in the nitric oxide synthase inhibition-induced hypertension model.

Magnesium has been implicated in the pathogenesis of hypertension, but the role of its intracellular levels in cardiovascular diseases is not clear yet. We investigated the relationships of low concentrations of serum magnesium (sMg) and intracellular Mg (iMg) with clinical and vascular parameters. Thiazide-treated hypertensive women were separated into two groups according to lower (<2.0 mg/dL) or normal (≥2.0 mg/dL) sMg concentrations. The same patients were later divided according to lower (<3.75 mg/dL erythrocytes) and normal (≥3.75 mg/dL erythrocytes) iMg concentrations. Carotid ultrasound, radial applanation, and peripheral arterial tonometry were performed in all patients. Low sMg levels were associated with increased Framingham Risk Score (16% ± 3% vs 11% ± 1%; P = .024), higher systolic (148 ± 7 vs 135 ± 3 mm Hg; P = .049) and diastolic (91 ± 3 vs 84 ± 2 mm Hg; P = .042) blood pressure, and carotid intima-media thickness (0.92 ± 0.09 vs 0.76 ± 0.02 mm; P = .023). Low concentrations of iMg were related to wave reflection parameters such as increased augmentation pressure (20 ± 2 vs 15 ± 1 mm Hg; P = .032) and augmentation index (43% ± 2% vs 33% ± 2%; P = .004). In conclusion, in these diuretic-treated hypertensive women, low sMg was associated with higher blood pressure values, and more intense wave reflection were closely linked to iMg depletion, processes that might contribute to hypertension and other cardiovascular risk factors., (Copyright © 2013 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Magnesium intake of 500 mg/d to 1000 mg/d may reduce blood pressure (BP) as much as 5.6/2.8 mm Hg. However, clinical studies have a wide range of BP reduction, with some showing no change in BP. The combination of increased intake of magnesium and potassium coupled with reduced sodium intake is more effective in reducing BP than single mineral intake and is often as effective as one antihypertensive drug in treating hypertension. Reducing intracellular sodium and calcium while increasing intracellular magnesium and potassium improves BP response. Magnesium also increases the effectiveness of all antihypertensive drug classes. It remains to be conclusively proven that cardiovascular disease such as coronary heart disease, ischemic stroke, and cardiac arrhythmias can be prevented or treated with magnesium intake. Preliminary evidence suggests that insulin sensitivity, hyperglycemia, diabetes mellitus, left ventricular hypertrophy, and dyslipidemia may be improved with increased magnesium intake. Various genetic defects in magnesium transport are associated with hypertension and possibly with cardiovascular disease. Oral magnesium acts as a natural calcium channel blocker, increases nitric oxide, improves endothelial dysfunction, and induces direct and indirect vasodilation., (© 2011 Wiley Periodicals, Inc.)

Project: Excessive bioavailability of Zn either due to genetic predisposition or its high concentration in diet has been linked to increase in the prevalence of hypertension (HT) implicating the resultant deficiencies of Cu and Mg as its cause in some populations. To combat their nutritional deficiencies, a modified poultry egg (ME(Psi)) was designed containing higher amounts of Cu, Mg and other antioxidants (vitamin E and linolenic acid) in their optimized concentrations. Prior to its human clinical trials, its efficacy was tested in Zn induced HT Wistar rat model in the present study., Procedure: In one set, the rats were fed on equicaloric semi-synthetic basal diet containing 20 mg Zn/kg diet (control diet-I, control group-I), Zn-induced-hypertensive-diets-II and III (Zn-HT-diet-II and Zn-HT-diet-III) containing 40 and 80 mg Zn/kg diet (groups-II and III) for 180 days. In another set, the rats were initially fed Zn-HT-diet-II and Zn-HT-diet-III for 90 days and then shifted to ME(Psi) mixed Zn-HT-diet-II and III designated as groups-IIME and IIIME fed for another 90 days completing 180 days of feeding., Results: The results revealed that increase in systolic pressure (SP) and heart rates (HR) were Zn concentration dependent and coincided well with higher serum Zn, Cu, Mg, aldosterone, cortisol, dyslipidemia and higher Zn, and low Cu and Mg concentrations in liver of groups-II and III rats. On feeding ME(Psi) mixed diets, a significant reduction in SP and HR were linked with decrease in serum Zn, Cu, Mg, aldosterone, cortisol and blood lipid profile along with fall in Zn and rise in Cu and Mg concentrations in liver of groups-IIME and IIIME approaching closer to control group-I., Conclusion: This study makes the basis for human clinical trials of ME(Psi) on HT patients who exhibit high Zn, Cu and Mg in their blood serum., (Copyright 2010 Elsevier GmbH. All rights reserved.)

Unlabelled: Comprehensive analytical review of 44 human studies in 43 publications of oral Magnesium (Mg) therapy for hypertension (HT) shows Mg supplements may enhance the blood-pressure (BP) lowering effect of anti-hypertensive medications (medications) in Stage 1 HT subjects. 9 studies conducted on subjects treated with medications continuously >/= 6 months (with /= 4 weeks within 6 months pre-study. Of the 4 remaining studies showing no BP change at these high Mg doses, two had large placebo effect, a third one had significant baseline discrepancies between Mg-test and placebo groups, and the fourth showed a significant decrease in DBP but not SBP. Thirteen studies on normotensive subjects, both treated and untreated with medications, showed no significant BP lowering effect with oral Mg therapy up to 25 mmol/day (607 mg)., Conclusions: Mg supplements above RDA may be necessary to significantly lower high blood pressure in Stage I HT unless subjects have been continuously treated with anti-HT medications >/= 6 months. Such medication use may lower by half the oral Mg dose needed to significantly decrease high blood pressure. Oral Mg therapy may have no effect in studies with normotensive subjects. Study of oral Mg therapy for severe or complicated hypertension has been neglected. Often the first cardiovascular risk factor to present, high blood pressure may be an early opportunity to correct poor Mg status and its possible complications including cardiovascular disease, respiratory diseases, and type 2 diabetes. Such preventive potential encourages quantification of these findings and testing of these hypotheses with a meta-analysis using categories elucidated by this preliminary study and finally would warrant a call for a prospective study.

Background: Accumulating evidence implicates a role of Mg(2+) in the pathophysiology of essential hypertension. Previous studies evaluating the antihypertensive efficacy of Mg(2+) supplementation gave contradictory results. This study aimed to investigate the effect of oral Mg(2+) supplementation on 24-h blood pressure (BP) and intracellular ion status in patients with mild hypertension., Methods: A total of 48 patients with mild uncomplicated hypertension participated in the study. Among them, 24 subjects were assigned to 600 mg of pidolate Mg(2+) daily in addition to lifestyle recommendations for a 12-week period and another 24 age- and sex-matched controls were only given lifestyle recommendations. At baseline and study-end (12 weeks) ambulatory BP monitoring, determination of serum and intracellular ion levels, and 24-h urinary collections for determination of urinary Mg(2+) were performed in all study subjects., Results: In the Mg(2+) supplementation group, small but significant reductions in mean 24-h systolic and diastolic BP levels were observed, in contrast to control group (-5.6 +/- 2.7 vs. -1.3 +/- 2.4 mm Hg, P < 0.001 and -2.8 +/- 1.8 vs. -1 +/- 1.2 mm Hg, P = 0.002, respectively). These effects of Mg(2+) supplementation were consistent in both daytime and night-time periods. Serum Mg(2+) levels and urinary Mg(2+) excretion were significantly increased in the intervention group. Intracellular Mg(2+) and K(+) levels were also increased, while intracellular Ca(2+) and Na(+) levels were decreased in the intervention group. None of the intracellular ions were significantly changed in the control group., Conclusion: This study suggests that oral Mg(2+) supplementation is associated with small but consistent ambulatory BP reduction in patients with mild hypertension.

Among toxicities associated with molecular targeted agents (MTA), cardiovascular toxicities remain largely unknown or underestimated. Their frequency is variable and dependent on the compound. A high incidence of hypertension, symptomatic or asymptomatic left ventricular systolic dysfunction, acute coronary syndrome, arterial and venous thrombosis has been observed in patients receiving MTA. One of the most threatening complications of angiogenic inhibitors (AI) could be QT prolongation with the risk of torsade de pointes (TdP) and sudden death. QT prolongation and torsade de pointes accounted for 29% of cardiac and non-cardiac post-marketing withdrawals. The assessment of the effects of drugs on cardiac repolarization is the subject of recent guidelines and recommendations. Regulatory agencies now require practically every new pharmaceutical compound to undergo a thorough investigation of its propensity to modify cardiac repolarization. To reduce the incidence of QT prolongation and torsade de pointes in patients receiving AI, cancer patients should be closely monitored while receiving AI.

The increasing evidence for the clinical relevance of altered magnesium metabolism to states of altered insulin resistance confirms the role of magnesium deficit as a possible underlying common mechanism of the "insulin resistance" of hypertension and altered glucose tolerance. The pioneer work of Lawrence M. Resnick and his group using the cellular ion-based approach that we are only partially presenting here has consistently contributed to the progress of the field, demonstrating (a) the critical importance of magnesium metabolism in regulating insulin sensitivity as well as vascular tone, and blood-pressure homeostasis; (b) that magnesium deficiency, defined on the basis of intracellular free magnesium levels, and or serum ionized magnesium is a common feature of both diabetic and hypertensive states as well as various other cardiovascular and metabolic processes and aging; (c) the ability of environmental factors such as dietary nutrient-sugar and mineral content to alter the set point of steady-state cell ion activity; and (d) that magnesium supplementation is indicated in conditions associated with magnesium deficit although well-designed therapeutic trials of magnesium in essential hypertension and type 2 diabetes mellitus are needed in the near future.

Background: Epidemiological evidence on the effects of magnesium on blood pressure is inconsistent. Metabolic and experimental studies suggest that magnesium may have a role in the regulation of blood pressure., Objectives: To evaluate the effects of magnesium supplementation as treatment for primary hypertension in adults., Search Strategy: We searched the Cochrane Library, MEDLINE, EMBASE, Science Citation Index, ISI Proceedings, ClinicalTrials.gov, Current Controlled Trials, CAB abstracts, and reference lists of systematic reviews, meta-analyses and randomised controlled trials (RCTs) included in the review., Selection Criteria: Inclusion criteria were: 1) RCTs of a parallel or crossover design comparing oral magnesium supplementation with placebo, no treatment, or usual care; 2) treatment and follow-up >/=8 weeks; 3) participants over 18 years old, with raised systolic blood pressure (SBP) >/=140 mmHg or diastolic blood pressure (DBP) >/=85 mmHg; 4) SBP and DBP reported at end of follow-up. We excluded trials where: participants were pregnant; received antihypertensive medication which changed during the study; or magnesium supplementation was combined with other interventions., Data Collection and Analysis: Two reviewers independently abstracted data and assessed trial quality. Disagreements were resolved by discussion or a third reviewer. Random effects meta-analyses and sensitivity analyses were conducted., Main Results: Twelve RCTs (n=545) with eight to 26 weeks follow-up met our inclusion criteria. The results of the individual trials were heterogeneous. Combining all trials, participants receiving magnesium supplements as compared to control did not significantly reduce SBP (mean difference: -1.3 mmHg, 95% CI: -4.0 to 1.5, I(2)=67%), but did statistically significantly reduce DBP (mean difference: -2.2 mmHg, 95% CI: -3.4 to -0.9, I(2)=47%). Sensitivity analyses excluding poor quality trials yielded similar results. Sub-group analyses and meta-regression indicated that heterogeneity between trials could not be explained by dose of magnesium, baseline blood pressure or the proportion of males among the participants., Authors' Conclusions: In view of the poor quality of included trials and the heterogeneity between trials, the evidence in favour of a causal association between magnesium supplementation and blood pressure reduction is weak and is probably due to bias. This is because poor quality studies generally tend to over-estimate the effects of treatment. Larger, longer duration and better quality double-blind placebo controlled trials are needed to assess the effect of magnesium supplementation on blood pressure and cardiovascular outcomes.

Magnesium is the second most abundant intracellular cation, and the important element that has numerous biological functions in the cardiovascular system. Furthermore, magnesium acts as calcium antagonist, regulates the calcium metabolism, and finally participates in blood pressure control. Although the evidence linking magnesium intake to the prevention of cardiovascular diseases was gathered, data from clinical studies about the magnesium usage in hypertension therapy have not been conclusive. The present review discusses the novel molecular and pharmacological effects of magnesium on cardiovascular systems and the implications in the clinical hypertension therapy based on the evaluating of patients' magnesium status.

Human essential hypertension is a complex, multifactorial, quantitative trait under polygenic control. Although the exact etiology is unknown, the fundamental hemodynamic abnormality in hypertension is increased peripheral resistance, due primarily to changes in vascular structure and function. These changes include arterial wall thickening, abnormal vascular tone and endothelial dysfunction and are due to alterations in the biology of the cellular and non-cellular components of the arterial wall. Many of these processes are influenced by magnesium. Small changes in magnesium levels may have significant effects on cardiac excitability and on vascular tone, contractility and reactivity. Accordingly magnesium may be important in the physiological regulation of blood pressure whereas perturbations in cellular magnesium homeostasis could play a role in pathophysiological processes underlying blood pressure elevation. For the most part, epidemiological and experimental studies demonstrate an inverse association between magnesium and blood pressure and support a role for magnesium in the pathogenesis of hypertension. However data from clinical studies have been less convincing and the therapeutic value of magnesium in the prevention and management of essential hypertension remains unclear. In view of the still ill-defined role of magnesium in clinical hypertension, magnesium supplementation is advised in those hypertensive patients who are receiving diuretics, who have resistant or secondary hypertension or who have frank magnesium deficiency. A magnesium-rich diet should be encouraged in the prevention of hypertension, particularly in predisposed communities because of the other advantages of such a diet in prevention. The clinical aspect that has demonstrated the greatest therapeutic potential for magnesium in hypertension, is in the treatment of pre-eclampsia and eclampsia. The present review discusses the role of magnesium in the regulation of vascular function and blood pressure and the implications in mechanisms underlying hypertension. Alterations in magnesium regulation in experimental and clinical hypertension and the potential antihypertensive therapeutic actions of magnesium will also be addressed.

We and others have shown that inhibition of cardiovascular muscle (CVM) cell Na+,K-ATPase activity (NKPTA) due to increased level of endogenous sodium potassium pump inhibitor (SPI) is involved in the mechanism of volume expanded (VE) experimental and human essential hypertension (HT). Since diets fortified with very high potassium (K) or very high magnesium (Mg) decrease blood pressure (BP), we have examined the effect of a moderate increase in dietary K alone and a moderate increase in dietary K and Mg on plasma levels of SPI, CVM cell NKPTA, and BP in reduced renal mass (RRM)-salt HT rats, a classical model of VE HT. Seventy Percent-RRM rats were divided in four dietary groups, (1) Na free and normal K and Mg (0Na-K-Mg); (2) normal Na, K and Mg (Na-K-Mg); (3) normal Na and high K (2 x normal), and normal Mg (Na-2K-Mg); and (4) normal Na and high K (2 x normal), and high Mg (2 x normal) (Na-2K-2Mg). As expected, compared to control 0Na-K-Mg rats, Na-K-Mg rats developed HT. Blood pressure increased significantly less in Na-2K-Mg rats whereas, BP did not increase in Na-2K-2Mg rats. Hypertension in NA-K-Mg rats was associated with an increase in plasma SPI and digitalis like factor (DIF) and a decrease in renal and myocardial NKPTA. However, doubling the Mg along with K in the diet (Na-2K-2Mg) normalized SPI and DIF and increased myocardial and renal NKPTA, compared to control 0Na-K-Mg rats. Also, compared to 0Na-K-Mg rats, water consumption, urine excretion, urinary sodium excretion urinary potassium excretion (U(Na)V), and (U(K)V) increased in the other three groups, more so in Na-2K-2Mg rats. These data show that K and Mg have additive effects in preventing an increase in SPI, thus probably preventing the BP increase in RRM rats.

This pilot study was aimed at investigating the hypotensive potential of hawthorn extract and magnesium dietary supplements individually and in combination, compared with a placebo. Thirty-six mildly hypertensive subjects completed the study. At baseline, anthropometric and dietary assessment, as well as blood pressure measurements were taken at rest, after exercise and after a computer 'stress' test. Volunteers were then randomly assigned to a daily supplement for 10 weeks of either: (a) 600 mg Mg, (b) 500 mg hawthorn extract, (c) a combination of (a) and (b), (d) placebo. Measurements were repeated at 5 and 10 weeks of intervention. There was a decline in both systolic and diastolic blood pressure in all treatment groups, including placebo, but ANOVA provided no evidence of difference between treatments. However, factorial contrast analysis in ANOVA showed a promising reduction (p = 0.081) in the resting diastolic blood pressure at week 10 in the 19 subjects who were assigned to the hawthorn extract, compared with the other groups. Furthermore, a trend towards a reduction in anxiety (p = 0.094) was also observed in those taking hawthorn compared with the other groups. These findings warrant further study, particularly in view of the low dose of hawthorn extract used., (Copyright 2002 John Wiley & Sons, Ltd.)

In most hypertensive rat models, serum total cholesterol is typically low and the cholesterol is primarily in the HDL rather than the LDL fraction. This difference from humans usually makes these animals unsuitable for experimental atherosclerosis studies. In the present study, we induced severe hypercholesterolemia including a 10-fold increase in serum LDL cholesterol, endothelial dysfunction and hypertension as well as vascular and renal damage in obese Zucker rats by feeding a human-type high fat, high cholesterol and high salt diet (butter 18, cholesterol 1 and NaCl 6 g/100 g dry weight). Supplementation of this atherogenic diet with plant sterols (1 g/100 g) and replacing the NaCl partially by calcium, magnesium and potassium effectively prevented the diet-induced increases in total and LDL cholesterols and 24-h systolic and mean blood pressures, and markedly improved endothelial function. Plant sterols and the minerals also protected against vascular and renal damage and extended the life span of the obese Zucker rats by 60% compared with the rats fed the atherogenic diet. Our findings suggest that human-type cardiovascular disorders can be induced in obese Zucker rats by feeding a human-type atherogenic diet. This seems to be a suitable animal model for experimental studies on atherosclerosis and hypertension as well as for evaluating new dietary approaches to reducing cardiovascular risk.

Objectives: Although magnesium is now the drug of choice for the prevention of eclamptic seizures only few studies have evaluated whether magnesium may reduce blood pressure in pregnancies complicated with hypertension., Methods: A total of 33 patients with pregnancy-induced hypertension were randomized to either magnesium or methyldopa treatment. Of these 16 received magnesium and 17 methyldopa. The treatment comprised a 48-hour magnesium infusion followed by oral magnesium tablets until 3 days after delivery or 250 mg methyldopa 4 times a day in a similar period., Results: Patients treated with magnesium had 1 day after inclusion a statistically significantly lower systolic blood pressure compared to the level in the methyldopa group (138.1 +/- 11 vs. 147.6 +/- 11 mm Hg; p < 0.05), but no difference was observed in diastolic blood pressure (92.0 +/- 6.6 vs. 96.0 +/- 10.1 mm Hg; NS). From the 5th day of inclusion and until delivery both systolic and diastolic blood pressure were significantly lower in the magnesium group (p < 0.05). Including all blood pressure measurements in a single analysis showed that both systolic (138 +/- 13 vs. 148 +/- 15 mm Hg; p < 0.0001) and diastolic (92 +/- 10 vs. 94 +/- 10 mm Hg; p < 0.05) blood pressure were lower in the magnesium group compared to the methyldopa group. There was no difference between the two groups regarding gestational age at delivery, birth weight, Apgar scores and pH in umbilical cord blood., Conclusion: This preliminary study demonstrates that magnesium treatment lowers blood pressure in pregnancies complicated with hypertension. The effect is without any adverse effect on maternal and neonatal well-being., (Copyright 2000 S. Karger AG, Basel)

The influence of a mineral salt on 24-h ambulatory blood pressure (BP) monitoring was studied in 20 elderly hypertensive subjects residing in an old peoples home. Ordinary table and cooking salt was substituted with a special Na-reduced, K-, Mg-, and l-lysine HCl-enriched mineral salt (Pansalt(R)) for 6 months. Antihypertensive therapy was uninterrupted. An ambulatory BP monitor (Suntech Accutracker) measured BP every 20 min during the day and every 30 min at night, before and 6 months after starting the diet. Nine patients (45%) decreased both systolic and diastolic BP significantly: systolic BP fell from 154.92 +/- 33.67 mm Hg to 143. 45 +/- 53.1 mm Hg (P < or = 0.01) during the daytime from 6 am to midnight; and from 139.80 +/- 32.84 mm Hg to 137.87 +/- 31.17 mm Hg (P < or = 0.01) from midnight to 6 am. Diastolic BP fell from 85.34 +/- 24.85 mm Hg to 70.29 +/- 18.31 mm Hg (P < or = 0.01) during the daytime from 6 am to midnight; and from 77.1 +/- 22.92 mm Hg to 67.76 +/- 15. 63 mm Hg (P < or = 0.01) at night. Blood pressure in the other 11 subjects showed no improvement. Heart rate also fell in the subjects, from 69.44 +/- 21.62 beats per minute (bpm) to 66.94 +/- 11.51 bpm (< or = 0.01) during the day, and from 61.28 +/- 12.82 bpm to 60.43 +/- 10.33 bpm (P < or = 0.01) during the night. It is concluded that decreased intake of Na and increased intake of both K and Mg can be useful in controlling high BP.

This study evaluated the effects of magnesium supplementation on the development of hypertension in spontaneously hypertensive rats (SHR) and assesses the actions of magnesium on extracellular and intracellular Ca2+, Na+, and K+ status. Ten-week-old SHR (n = 72) and Wistar-Kyoto rats (WKY) (n = 60) were divided into four groups: WKY, Mg-WKY (WKY receiving 650 mg/L Mg(2+)supplementation), SHR, and Mg-SHR (SHR receiving Mg2+). Rats were studied for 17 weeks. Serum and erythrocyte Mg2+ and Ca2+ (measured by atomic absorption spectroscopy) and Na+ and K+ (measured by flame photometry) were determined every 3 or 4 weeks. From 13 weeks of age, blood pressure (BP) was significantly elevated in SHR compared with age-matched WKY. BP was reduced (P < .01) in SHR after 10 weeks of Mg2+ supplementation and at 27 weeks of age, BP in SHR was 218 (12 mm Hg v 184 +/- 9 mm Hg) in Mg-SHR. From 18 weeks of age, serum and intracellular Mg2+ levels were significantly lower (P < .05) and from 21 weeks of age, erythrocyte Ca2+ was significantly higher in SHR than in WKY. Mg2+ supplementation normalized intracellular Mg2+ and Ca2+ concentrations in SHR. BP was inversely correlated with erythrocyte Mg2+ (r = -0.74, P < .01) and positively correlated with erythrocyte Ca2+ (r = 0.78, P < .001). In conclusion, long-term Mg2+ supplementation significantly attenuates, but does not prevent, the development of hypertension in SHR. Furthermore, intracellular Mg2+ deficiency and Ca2+ overload in SHR are normalized by Mg2+ treatment.

A parallel controlled clinical trial was carried out to investigate the effect on blood pressure (BP) of replacing normal salt with mineral salt in seasonings. After a 2-wk run-in period, 21 subjects (10 men and 11 women; age, 66.0+/-7.6 yr) were given mineral salt in seasonings instead of normal salt [mineral salt (MS) group], while 20 subjects (10 men and 10 women; age, 65.9+/-7.4 yr) continued to receive normal salt in seasonings [regular salt (RS) group] for the next 5 wk in the experimental (E) period. In the MS group, systolic (S) and diastolic (D) BP decreased significantly from 134.7+/-17.2/77.2+/-9.7 at baseline (week 0) to 127.3+/-12.0/73.5+/-8.9 mmHg at the end of the E period (week 5), and the reductions in both SBP and DBP were larger in hypertensive subjects than in normotensive subjects in the MS group. The serum sodium and chloride concentrations decreased significantly, while the serum potassium and HDL-cholesterol concentrations increased significantly at week 5. The 24-h urinary sodium excretion decreased, and the 24-h potassium and magnesium excretions increased significantly from week 0 to week 5 in the MS group. In contrast, SBP, DBP, serum chemistry, and urinary electrolyte excretion did not change significantly in the RS group. These findings suggest that the excessive salt content and insufficient potassium and magnesium content of the present Japanese diet could be easily and safely corrected by replacing seasonings prepared with regular salt with those prepared with mineral salt.

Fifteen patients with uncomplicated mild to moderate primary hypertension (7 males, 8 females, age range 36-65 years) were submitted to a double blind randomized crossover study, receiving MgO 3 times a day at a daily dose of 1.0 g (600 mg/day of magnesium) and placebo for a period of 6 weeks. This was to test the effects of oral magnesium supplementation on blood pressure and sodium, potassium, calcium and magnesium intraerythrocyte concentrations. Concomitantly, plasma renin activity and serum aldosterone was also measured. Oral magnesium reduced significantly the systolic (delta = -7.6 mmHg, P < 0.05); diastolic (delta = -3.8 mmHg, P < 0.01) and mean blood pressure (delta = -5.9 mmHg, P < 0.01). After magnesium supplementation intraerythrocyte sodium concentration was reduced (delta = -0.55 mEq/l per cell, P < 0.01) and intraerythrocyte magnesium concentration was increased (delta = 1.20 mg/dl per cell, P < 0.01). The diminution of the blood pressure correlated positively with the reduction in intraerythrocyte sodium (r = 0.66, P < 0.01) after magnesium. However, our results have shown that the blood pressure response to oral magnesium was not homogeneous. Forty percent of our patients had their blood pressure effectively controlled (more than 10 mmHg reduction in mean blood pressure), being the hypotensive effect more evident in patients with recent hypertension and in those where the reduction in intraerythrocyte sodium was significantly greater than in the non-responder individuals. Intraerythrocyte potassium and calcium, serum aldosterone, plasma renin activity and urinary sodium excretion were maintained unchanged after magnesium supplementation. These data showed that oral magnesium supplementation may reduce the blood pressure, which can be partially explained by the decrease in intracellular sodium and augment in intracellular magnesium.

We have previously demonstrated that modest sodium restriction has a hypotensive effect in hypertensive diabetic subjects. A randomised blind controlled study has therefore been performed to study the effect of replacement of added salt intake using a salt substitute (50% NaCl, 40% KCL, 10% Mg2+, supplied by Cederroth, Sweden), compared to added whole salt intake over a 9 month period of 40 hypertensive Type II diabetic subjects (mean age 62.5 +/- 7.8 years; 24 males and 16 females). After 3 months, there was a significant reduction in systolic blood pressure (SBP) in the salt substitution group (163.2 +/- 24.2 to 153.6 +/- 20.8 mm Hg; P < 0.03) which was maintained at 9 months, when compared to the whole salt group (151.5 +/- 20.6 vs 173 +/- 18.9 mm Hg; P < 0.05). No significant changes were observed in mean weight, fasting lipid or insulin levels or diabetic control (measured by glycosylated haemoglobin). A greater number of patients were withdrawn during the study period owing to consistent BP > 160/95 in the whole salt group (n = 10) compared to salt substitute (n = 4). No significant changes were observed in diastolic pressure, 24-h urine sodium or magnesium excretion, but urine potassium was significantly increased in the salt substitute group (58.8 to 77.3: P < 0.05). The results of this study suggest that substitution of sodium, by potassium and magnesium, produces a clinically significant reduction in SBP in hypertensive Type II diabetic patients, and should be a useful antihypertensive therapy in this patient group.

Dietary intakes of potassium, calcium, and magnesium have each been reported to lower blood pressure, but the extent of blood pressure reduction in epidemiological studies and clinical trials has tended to be small and inconsistent. We hypothesized that combinations of these mineral supplements would lower blood pressure and that the reductions would be greater than that usually reported in studies of each cation alone. One hundred twenty-five patients 82 men and 43 women) with untreated mild or borderline hypertension were randomly assigned to daily treatment with one of the following four regimens: 60 mmol potassium and 25 mmol (1000 mg) calcium, 60 mmol potassium and 15 mmol (360 mg) magnesium, calcium and magnesium, or placebo. Standardized clinic blood pressure measurements were obtained on 3 days at baseline and after 3 and 6 months of treatment. At baseline, systolic and diastolic blood pressures (mean +/- SD) were 139 +/- 12 and 90 +/- 4 mm Hg, respectively, and dietary intakes of potassium, calcium, and magnesium were 77 +/- 32, 19 +/- 13, and 12 +/- 52 mmol/d, respectively. The mean differences (with 95% confidence intervals) of the changes in systolic and diastolic blood pressures between the treatment and placebo groups were not significant: -0.7 (-4.3 to +2.9) and -0.4 (-2.9 to +2.1) for potassium and calcium, -1.3 (-4.4 to +1.8) and 0.4 (-2.5 to +3.3) for potassium and magnesium, and +2.1 (-1.8 to +6.0) and +2.2 (-1.0 to +5.4) for calcium and magnesium. In conclusion, this trial provides little evidence of an important role of combinations of cation supplements in the treatment of mild or borderline hypertension.

The present study examines the effects of dietary magnesium on the development of hypertension and hypertensive vascular lesions in deoxycorticosterone acetate and salt induced (DOCA-salt) and 2 kidney one clip (2K1C) hypertensive as well as normotensive control rats. Animals received a regular (0.12% Mg), high (0.4% Mg) or low (0.03% Mg) magnesium diet for 6 wks. Dietary magnesium did not alter the growth or blood pressure in control, DOCA-salt and 2K1C rats even though the plasma magnesium concentration was significantly altered by the diets (ANOVA, p < 0.05 in control, DOCA-salt and 2K1C, respectively). Dietary magnesium did not alter the urinary potassium excretion, plasma sodium, potassium, total calcium concentration and plasma renin activity in any group, while the high magnesium diet significantly increased the urinary sodium excretion in DOCA-salt (p < 0.05) but not in control and 2K1C rats when compared with the regular magnesium diet. In histological studies, dietary magnesium did not alter the percentage media area of intramyocardial arteries, or glomerular and renal arterial and arteriolar lesions in DOCA-salt and 2K1C rats. This study suggests that moderate alterations of dietary magnesium do not modify blood pressure in normotensive control, DOCA-salt and 2K1C hypertensive rats, nor do they modify vascular disease in these 2 hypertensive models.

At present, magnesium treatment is employed routinely in the treatment of hypertension induced by pregnancy (PIH) and preeclampsia in USA with the object of preventing seizures. In USA the treatment of election consists of intravenous infusion of large doses of magnesium sulphate in order to obtain a therapeutic concentration. The anticonvulsive mode of action of magnesium is only partially understood. Magnesium is presumed to block the neuromuscular transmission but a central effect cannot be excluded. Treatment with magnesium has, in addition, an antihypertensive effect. The effect of magnesium on the blood pressure is probably a direct vasodilatory effect which explains the ability of magnesium to reduce the maternal blood pressure. Probably the same mode of action is responsible for the relaxing effect of magnesium on the vascular tone in the umbilical and placental vessels. This can probably explain the favourable effect of magnesium on the birth weight. Even if magnesium treatment implies a potential risk for neonatal hypermagnesemia and hypocalcaemia, only few side effects have been reported.

Seventeen patients with a diastolic blood pressure over 90 mm Hg were recruited from a running health screening program to participate in a double blind cross-over study of magnesium supplementation (15 mmol Mg2+/day (Emgesan, Kabi Pharmacia) for 3 weeks, followed by 30 mmol Mg2+/day for another 3 weeks, finishing with 40 mmol Mg2+/day for a final 3 weeks). A significant decrease in the mean systolic blood pressure was recorded from 154.0 +/- 10.7 mm Hg to 146.1 +/- 16.9 mm Hg (P = .031) while the mean diastolic blood pressure decreased from 100.2 +/- 4.2 mm Hg to 92.0 +/- 6.6 mm Hg (P = .0001).

In pregnancy calcium antagonism is of great importance. The uterus-relaxing properties of verapamil are well known, diltiazem shows an excellent tokolytic efficacy and is also effective as hypotensive in pregnancy-induced hypotension. In contrast to verapamil and diltiazem the dihydropyridines were not clinically successful as tokolytic or hypotensive in pregnancy. Magnesium is a therapy of first choice in the EPH-gestosis.

To evaluate the antihypertensive and hormonal effects of oral magnesium supplementation, 17 inpatients with untreated, uncomplicated mild-to-moderate essential hypertension (EH) and 8 age-matched normotensive controls (controls) were given MgO orally 3 times a day at a daily dose of 1.0 g (0.6 g per day as Mg) for a period of 2 weeks. Supplementation of MgO elicited a significant fall in averaged mean blood pressure calculated with a 24-h ambulatory blood pressure monitoring system (MBP) in EH from a baseline value of 104.3 +/- 12.2 to 99.5 +/- 11.6 mmHg (p < 0.05), while controls remained unaltered from a baseline value of 85.1 +/- 11.5 to 84.5 +/- 13.3 mmHg. The percentage reductions in systolic and diastolic blood pressures were similar during daytime and nighttime in EH. According to the extent of reduction in MBP with magnesium supplementation, EH patients were divided into 2 groups, responder and nonresponder. The level of plasma renin activity (PRA) in the responder group was significantly higher than that of the nonresponder group (p < 0.05). After 2 weeks of magnesium supplementation, the plasma level of Na+, K(+)-ATPase inhibitory activity (PATPI), defined as equivalency to ouabain, was reduced significantly from 0.75 +/- 0.54 to 0.40 +/- 0.30 mumol ouabain/ml (p < 0.05) in the responder group, while it remained unaltered in controls and the nonresponder group. PRA, plasma aldosterone concentration, urinary epinephrine and norepinephrine excretion, and urinary sodium excretion did not change significantly in either control subjects or EH (responder and nonresponder groups). A significant negative correlation existed between the pretreatment PRA and changes in MBP after magnesium supplementation in EH (r = -0.65, p < 0.01), and there was a significant positive correlation between changes in PATPI and changes in MBP as a whole (r = 0.41, p < 0.05). These results support the view that oral magnesium supplementation is a useful approach to treatment of patients with uncomplicated essential hypertension, especially those with high plasmas renin activity. It appears that magnesium suppresses circulating Na+,K(+)-ATPase inhibitory activity to attenuate vascular tone, and thereby reduces blood pressure in EH.

In newly-diagnosed untreated (n = 24) and thiazide treated (n = 18) hypertensive patients erythrocyte ion content and plasma ion and metabolite levels were determined. Thiazide treated patients had lower arterial blood pressure, plasma ion levels, erythrocyte magnesium and potassium content but higher fasting plasma insulin (66 +/- 7 v 87 +/- 8 pmol/L P < .02), triglycerides (1.88 +/- 0.24 v 2.34 +/- 0.44 mmol/L P < .05), free fatty acids (0.68 +/- 0.11 v 0.81 +/- 0.18 mmol/L P < .05). Subsequently, in a double-blind fashion and in random order thiazide diuretic treated patients were assigned to two groups: the first (n = 9) taking magnesium (15.8 mmol/day) and the other (n = 9) a placebo. Each treatment period lasted 8 weeks. At the end of each treatment period, each patient underwent blood sampling for determination of erythrocyte ion content and plasma ion and metabolite levels and was submitted to an euglycemic hyperinsulinemic (1 mU/kg/min for 120 min) glucose clamp. In this latter test D-3-H glucose infusion and indirect calorimetry allowed determination of glucose turnover parameters and substrate oxidation respectively. Chronic magnesium administration (CMA) raised fasting plasma (0.79 +/- 0.03 v 0.83 +/- 0.02 mmol/L, P < .05) and erythrocyte (1.98 +/- 0.08 v 2.35 +/- 0.03 mmol/L, P < .01) magnesium content. Along with insulin infusion, CMA improved glucose uptake, glucose metabolic clearance rate, and oxidative glucose metabolism. In the multiple linear regression analysis of the pooled basal data (n = 42), erythrocyte magnesium content displayed an independent correlation with basal plasma insulin levels (t = -2.08, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Magnesium deficit may be considered as a cardiovascular risk because of its aetiopathogenic role in the genesis of atherogenous dyslipidaemias and the so-called "idiopathic" mitral valve prolapse. It does not, however, constitute a major antihypertensive factor, though it may sometimes be an accessory co-factor. Plasma magnesium is generally normal in untreated hypertensive patients and normotension is the rule during magnesium deficit. An inverse relationship between magnesium and renin in the plasma of hypertensives has not been confirmed. In practice, plasma magnesium seems to be related to the evolution of the disease. An inverse correlation between blood pressure and erythrocyte total and free magnesium levels has been observed in diverse selected populations but no adjustment has been made in these studies for important covariables. A weak positive association between blood pressure and erythrocyte free magnesium was lost in a multivariate regression analysis. As a rule there is no difference between erythrocyte, leucocyte, and lymphocyte magnesium in hypertensives and controls. More often no relation between urinary magnesium and blood pressure is observed. Daily urine magnesium may be increased with increased excretion of urine adrenaline. Epidemiological data on dietary magnesium, particularly in drinking water, should be carefully scrutinized: these studies do not establish a major role for magnesium as an antihypertensive factor but confirm the importance of magnesium deficit as a nephrocardiovascular risk factor and sometimes gives support for a role of magnesium as an antihypertensive cofactor. The use of magnesium-depleting drugs in hypertensive patients may induce magnesium depletion which must be palliated.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of chronic alcohol administration on blood pressure was investigated in 7-week-old Wistar rats. Tail-cuff blood pressure was significantly higher in rats who received 15% ethanol in drinking water than in control rats. Intracellular free calcium concentration of lymphocytes was increased, while magnesium concentration of erythrocyte, aorta, and skeletal muscle and erythrocyte ouabain-sensitive 22Na efflux rate constant (Kos) were decreased in alcohol-induced hypertensive rats but not in control rats. Extracellular fluid volume was also increased in alcohol-administered rats. Oral magnesium supplementation (1% MgO in rat chow) attenuated the development of alcohol-induced hypertension accompanied by increased magnesium concentration of erythrocyte, aorta, skeletal muscle, and Kos and decreased intraerythrocyte sodium concentration. Norepinephrine half-life time of the heart and spleen was also increased in magnesium-supplemented rats. Blood pressure significantly correlated positively with intracellular calcium concentration and extracellular fluid volume, negatively with magnesium concentration of erythrocyte, aorta, skeletal muscle, and Kos. These results suggest that increased intracellular calcium, which was partly due to magnesium depletion and suppressed sodium pump activity, and expanded body fluid volume had a possible role in the development of alcohol-induced hypertension. It is also suggested that oral magnesium supplementation had a hypotensive effect on alcohol-induced hypertension possibly through decreased intracellular sodium concentration caused by an activation of sodium pump and decreased sympathetic nervous activity.

The main objective of this clinical trial was to evaluate the effects of magnesium pidolate (15 mmol/day) on blood pressure at rest and during sympathetic stimulation induced by cold, isometric and tilt test; peripheral blood flow has been evaluated by strain-gauge plethysmography. Fourteen mild to moderate hypertensives (8 males, 6 females, age range 40-60 years) were randomly given magnesium or placebo in a double-blind parallel clinical trial for 6 months. In the actively treated group magnesium urinary excretion increased from 5.3 +/- 2 to 7.7 +/- 2 mmol/24 h, and serum magnesium changed from 0.9 +/- 0.1 to 1.0 +/- 0.2 mmol/l. On magnesium, BP changed at rest from 156/97 +/- 12/4 to 149/90 +/- 8/3 mm Hg, during cold pressor test from 169/105 +/- 9/6 to 174/105 +/- 15/4, during isometric exercise from 170/107 +/- 13/9 to 170/105 +/- 20/6, and during tilt test from 149/96 +/- 11/6 to 153/96 +/- 17/7 mm Hg. Similar changes were observed in the placebo group. Peripheral resistances were 14.7 +/- 4 and 9.8 +/- 2 PRU before and after magnesium, respectively. These data indicate that long-term magnesium pidolate supplementation does not affect blood pressure at rest and during sympathetic stimulation, despite a slight, nonsignificant reduction in forearm peripheral resistance.

Magnesium (Mg2+) has antagonistic properties to calcium (Ca2+) and has been termed the physiologic Ca2+ blocker. Synthetic Ca2+ channel blockers are extensively used as anti-hypertensive agents. It is hypothesised that when administered in combination synthetic Ca2+ channel blockers and Mg are synergistic in the treatment of hypertension.