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Objective: Current international guidelines recommend home blood pressure (BP) measurement and low sodium and high potassium intakes for the management of hypertension. We hypothesized that increased home BP measurement may result in more effective management of sodium and potassium intakes and BP., Methods: We examined associations of home BP measurement days with changes in the urinary sodium-to-potassium (Na/K) ratio, estimated salt and potassium intakes and BP. We included 209 healthy participants (mean age, 55.9 years; 56.5% women) from a prospective cohort study. We examined 1-year data on self-measured home BP and spot urine samples., Results: Median (interquartile range) days of home BP measurement was 324 (225-358) over 1-year. Baseline mean (SD) Na/K ratio, salt and potassium intakes, morning and evening SBP, and morning and evening DBP were 3.8 (2.3), 8.5 (1.9) g/day, 1833.5 (416.5) mg/day, 120.4 (14.0) mmHg, 118.2 (14.2) mmHg, 79.2 (10.1) mmHg, and 76.2 (10.1) mmHg, respectively. In multivariable-adjusted linear regression , β (standard error) per 10 days increase in number of home BP measurement were -0.031 (0.017) for Na/K ratio, -0.036 (0.015) for salt intake, -1.357 (2.797) for potassium intake, -0.178 (0.064) for morning SBP, -0.079 (0.041) for morning DBP, -0.109 (0.067) for evening SBP and -0.099 (0.045) for evening DBP. Additionally, relationships persisted for men and women, but changes in salt intake were more pronounced among participants taking antihypertensive medication (interaction P = 0.002)., Conclusion: Continuous measurement of home BP may lead not only to self-monitoring of BP, but also to declines in salt intakes and some BP indices., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Men with heart failure are reported to be less adherent to low-sodium diets than women are. One potential reason may be that men consume more food and, consequently, more sodium than women do., Objectives: The aims of this study were to compare dietary sodium intake, urine sodium excretion, and sodium density of diet consumed between men and women with heart failure and to determine whether sex moderated the relationship of kilocalories (kcals) consumed with dietary and urine sodium., Methods: A total of 223 patients with heart failure (mean age, 62 ± 12 years; 70% men, 46% New York Heart Association class III-IV) completed detailed 4-day food diaries and provided 24-hour urine sodium samples. To account for sodium density of food, dietary sodium and urine sodium were referenced to sodium per 1000 kcal., Results: On an absolute basis, men consumed 23% more kcals and 28% more sodium than women did; 24-hour sodium excretion was 16% higher in men than in women. There were no differences between men and women when dietary sodium and urinary sodium were referenced to 1000 kcal, indicating they consumed foods with similar sodium density. However, both moderation analyses showed that the dietary sodium intake of men and women with lower kcal intake was similar, whereas men with higher kcal intake consumed more sodium-dense foods than women did., Conclusion: The results suggest that the men with higher sodium intake than women had 2 reasons for nonadherence. They consumed more food and foods with higher sodium density than women did.

Background: Sodium-induced microcirculatory changes, endothelial surface layer alterations in particular, may play an important role in sodium-mediated blood pressure elevation. However, effects of acute and chronic sodium loading on the endothelial surface layer and microcirculation in humans have not been established. The objective of this study was to assess sodium-induced changes in blood pressure and body weight as primary outcomes and also in microvascular permeability, sublingual microcirculatory dimensions, and urinary glycosaminoglycan excretion in healthy subjects., Methods: Twelve normotensive males followed both a low-sodium diet (less than 50 mmol/day) and a high-sodium diet (more than 200 mmol/day) for eight days in randomized order, separated by a crossover period. After the low-sodium diet, hypertonic saline (5 mmol sodium/liter body water) was administered intravenously in 30 min., Results: Both sodium interventions did not change blood pressure. Body weight increased with 2.5 (95% CI, 1.7 to 3.2) kg (P < 0.001) after dietary sodium loading. Acute intravenous sodium loading resulted in increased transcapillary escape rate of I-labeled albumin (2.7 [0.1 to 5.3] % cpm · g · h; P = 0.04), whereas chronic dietary sodium loading did not affect transcapillary escape rate of I-labeled albumin (-0.03 [-3.3 to 3.2] % cpm · g · h; P = 1.00), despite similar increases of plasma sodium and osmolality. Acute intravenous sodium loading coincided with significantly increased plasma volume, as assessed by the distribution volume of albumin, and significantly decreased urinary excretion of heparan sulfate and chondroitin sulfate. These changes were not observed after dietary sodium loading., Conclusions: Our results suggest that intravenous sodium loading has direct adverse effects on the endothelial surface layer, independent of blood pressure.

Although reducing dietary salt consumption is the most cost-effective strategy for preventing progression of cardiovascular and renal disease, policy-based approaches to monitor sodium intake accurately and the understanding factors associated with excessive sodium intake for the improvement of public health are lacking. We investigated factors associated with high sodium intake based on the estimated 24-hour urinary sodium excretion, using data from the 2009 to 2011 Korea National Health and Nutrition Examination Survey (KNHANES). Among 21,199 adults (≥19 years of age) who participated in the 2009 to 2011 KNHANES, 18,000 participants (weighted n = 33,969,783) who completed urinary sodium and creatinine evaluations were analyzed in this study. The 24-hour urinary sodium excretion was estimated using Tanaka equation. The mean estimated 24-hour urinary sodium excretion level was 4349 (4286-4413) mg per day. Only 18.5% (weighted n = 6,298,481/3,396,973, unweighted n = 2898/18,000) of the study participants consumed less the 2000 mg sodium per day. Female gender (P < 0.001), older age (P < 0.001), total energy intake ≥50 percentile (P < 0.005), and obesity (P < 0.001) were associated with high sodium intake, even after adjusting for potential confounders. Senior high school/college graduation in education and managers/professionals in occupation were associated with lower sodium intake (P < 0.001). According to hypertension management status, those who had hypertension without medication consumed more sodium than those who were normotensive. However, those who receiving treatment for hypertension consumed less sodium than those who were normotensive (P < 0.001). The number of family members, household income, and alcohol drinking did not affect 24-hour urinary sodium excretion. The logistic regression analysis for the highest estimated 24-hour urinary sodium excretion quartile (>6033 mg/day) using the abovementioned variables as covariates yielded identical results. Our data suggest that age, sex, education level, occupation, total energy intake, obesity, and hypertension management status are associated with excessive sodium intake in Korean adults using nationally representative data. Factors associated with high sodium intake should be considered in policy-based interventions to reduce dietary salt consumption and prevent cardiovascular disease as a public health target.

Our aim was to determine the frequency of orthostatic edema (OE) in patients with idiopathic intracranial hypertension (IIH). We evaluated 30 women with IIH for evidence of OE by comparing sodium and water excretion in the recumbent and standing postures and morning and evening body weights. Data were compared with findings in 30 women with OE, 22 weight-matched obese normal subjects, and 20 lean normal subjects. The effect of treatment with diuretics or diuretics plus sympathomimetic agents was compared. Seventy-seven percent of IIH patients had evidence of peripheral edema and 80% had significant orthostatic retention of sodium or water. Excretion of a standard saline load and of a tap water load was significantly impaired in the upright posture in the IIH and OE patients compared with the lean and obese normal subjects. Diuretic therapy induced weight loss (up to 9 kg) and decreased mean weight gain from morning to evening in 5 of 12 patients treated. In seven patients also treated with diuretics plus sympathomimetic drugs, the diuretic-induced morning weight loss and morning to evening weight gain were both significantly improved with the addition of sympathomimetic agents. Therapy reduced the frequency or severity of headaches in seven patients and reduced papilledema in four patients who received no other concurrent treatment for IIH. The orthostatic retention of sodium and water and the consequent edema is very similar in IIH and OE patients, suggesting a common pathogenesis for both disorders. Diuretic therapy, dietary salt and water restriction, and planned periods of recumbency merit study as a treatment for these patients.

Background: Sodium restriction has been widely used for treatment of hypertension and renal diseases. Whether sodium restriction can transform the circadian rhythm of blood pressure from nondipper to dipper is examined., Methods and Results: Patients (n=42) with essential hypertension were maintained on a high-sodium diet (12 to 15 g of NaCl per day) and a low-sodium diet (1 to 3 g/d) for 1 week each. On the last day of each diet, blood pressures were measured noninvasively every hour for 24 hours with an automatic oscillometric device. Twenty-one patients were classified as non-sodium sensitive whereas 21 were classified as sodium sensitive on the basis of a > or = 10% change in 24-hour mean arterial pressure caused by sodium restriction. Nocturnal blood pressure fall was significant in the non-sodium sensitive subjects but not in sodium-sensitive subjects. There was a significant interaction between sodium restriction and nocturnal fall in blood pressure only in the sodium-sensitive subjects, indicating that the degree of the nocturnal fall was affected by sodium restriction. Furthermore, changes in the nocturnal fall induced by sodium restriction had a positive relationship with sodium sensitivity (r=.38, P<.02) and a negative relationship with the nocturnal fall before sodium restriction (r=-.75, P<.0001)., Conclusions: These findings show the difference in nocturnal fall in blood pressure between the non-sodium sensitive and sodium-sensitive types of essential hypertension. The diminished nocturnal fall, recognized in the sodium-sensitive type, is restored by sodium restriction, indicating that the circadian rhythm of blood pressure shifted from a nondipper to a dipper pattern. On the other hand, the nocturnal fall is not affected by sodium restriction in the non-sodium sensitive type, and the circadian rhythm remains of the dipper variety.

Responses of renal nerve activity and urinary Na+ and Cl- excretion were examined in chronically instrumented conscious dogs through feedings of boiled rice with or without NaCl. The boiled rice (20 g/kg body wt) without NaCl did not influence plasma Na+ and Cl- concentrations, renal nerve activity, or urinary Na+ excretion but decreased urinary Cl- excretion. On the other hand, boiled rice containing NaCl (0.4 g/kg body wt) increased plasma Na+ (+3.8 +/- 0.7 meq/l) and Cl- (+3.0 +/- 1.5 meq/l) concentrations, then decreased renal nerve activity by 61 +/- 4%, and increased urinary Na+ and Cl- excretions. In dogs with hepatic denervation, a decrease in renal nerve activity, which was observed in intact dogs in response to the high-NaCl food intake, was completely abolished along with significant attenuation of postprandial natriuresis. That is, only 9 +/- 5% of the loaded Na+ and 7 +/- 3% of the loaded Cl- were excreted during 4 consecutive hours in hepatic-denervated dogs, whereas 36 +/- 5% of the loaded Na+ and 36 +/- 4% of the loaded Cl- were excreted in intact dogs. In dogs with renal denervation, postprandial natriuresis was also attenuated. These results indicate that the high-NaCl food intake elicits a decrease in renal nerve activity, the decrease is predominantly mediated by the hepatic nerves, and the decrease in renal nerve activity plays an important role in augmentation of urinary Na+ and Cl- excretion. Thus, the hepatorenal reflex may play an important role in controlling extracellular fluid homeostasis during food intake.

Besides the duration and severity of hypertension, several other factors have been shown to be related to left ventricular hypertrophy (LVH) in essential hypertension. The present study was conducted to examine the influence of salt sensitivity on LVH. Fifteen essential hypertensive ambulatory patients were submitted to a low-salt (30 mEq of Na/day for 7 days) and a high-salt (200 mEq of Na/day for 7 days) diet after 12 weeks on placebo. Daily urine collection was obtained during the whole study. After the placebo period, all patients were submitted to a complete clinical and laboratory investigation that included an echocardiogram (M-mode and two-dimensional). Five patients were salt-sensitive (mean blood pressure (BP) increase from the seventh day of the low- to the seventh day of the high-salt diet greater than 10%). No differences in weight, sex ratio, and duration of hypertension were obtained between salt-sensitive and -resistant patients. The initial BP was higher in the salt-sensitive patients. However, the difference was small and without statistical significance. The left ventricular weight was higher in the salt-sensitive than in salt-resistant patients (148 +/- 51 vs. 109 +/- 32 g/m2, p less than 0.05). The left ventricular end-diastolic diameter was also higher in the salt-sensitive patients (50 +/- 10 vs. 43 +/- 6 mm, p less than 0.05). The interventricular septum and posterior wall thicknesses were higher in salt-sensitive patients, although they did not reach statistical significance. In conclusion, salt-sensitive essential hypertensive patients are at a higher risk to develop LVH.