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The diagnosis and management of hypertension, a common cardiovascular risk factor among the general population, have been based primarily on the measurement of blood pressure (BP) in the office. BP may differ considerably when measured in the office and when measured outside of the office setting, and higher out-of-office BP is associated with increased cardiovascular risk independent of office BP. Self-measured BP monitoring, the measurement of BP by an individual outside of the office at home, is a validated approach for out-of-office BP measurement. Several national and international hypertension guidelines endorse self-measured BP monitoring. Indications include the diagnosis of white-coat hypertension and masked hypertension and the identification of white-coat effect and masked uncontrolled hypertension. Other indications include confirming the diagnosis of resistant hypertension and detecting morning hypertension. Validated self-measured BP monitoring devices that use the oscillometric method are preferred, and a standardized BP measurement and monitoring protocol should be followed. Evidence from meta-analyses of randomized trials indicates that self-measured BP monitoring is associated with a reduction in BP and improved BP control, and the benefits of self-measured BP monitoring are greatest when done along with cointerventions. The addition of self-measured BP monitoring to office BP monitoring is cost-effective compared with office BP monitoring alone or usual care among individuals with high office BP. The use of self-measured BP monitoring is commonly reported by both individuals and providers. Therefore, self-measured BP monitoring has high potential for improving the diagnosis and management of hypertension in the United States. Randomized controlled trials examining the impact of self-measured BP monitoring on cardiovascular outcomes are needed. To adequately address barriers to the implementation of self-measured BP monitoring, financial investment is needed in the following areas: improving education and training of individuals and providers, building health information technology capacity, incorporating self-measured BP readings into clinical performance measures, supporting cointerventions, and enhancing reimbursement.

We compared the impact of renal denervation (RDN) on blood pressures using results available from a recent comprehensive meta-analysis and an international registry. The meta-analysis summarized recent trials in which RDN was compared with control groups that were treated only with antihypertensive medication; the registry only included patients treated with RDN. Both publications presented pretreatment pressures and changes 6 months postbaseline. Significant reductions in office systolic pressure and 24 h ambulatory systolic pressure were observed in both groups of the meta-analysis and the registry. However, the magnitude of blood pressure reduction with RDN and medical treatment was comparable in both the meta-analysis and registry. RDN has not been shown to be superior to medical management of hypertension in this combined experience of nearly 2000 hypertensive patients.

A report from panel members appointed to the Eighth Joint National Committee titled "2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults" has garnered much attention due to its major change in recommendations for hypertension treatment for patients ≥60 years of age and for their treatment goal. In response, certain groups have opposed the decision to initiate pharmacologic treatment to lower blood pressure (BP) at systolic BP ≥150 mm Hg and treat to a goal systolic BP of <150 mm Hg in the general population age ≥60 years. This paper contains 3 sections-an introduction followed by the opinions of 2 writing groups-outlining objections to or support of maintaining this proposed strategy in certain at-risk populations, namely African Americans, women, and the elderly. Several authors argue for maintaining current targets, as opposed to adopting the new recommendations, to allow for optimal treatment for older women and African Americans, helping to close sex and race/ethnicity gaps in cardiovascular disease morbidity and mortality., (Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Orthostatic hypotension (OH) is the failure of cardiovascular reflexes to maintain blood pressure on standing from a supine or sitting position. Although OH may cause symptoms of dizziness or syncope, asymptomatic OH (AOH) is far more common and is an independent risk factor for mortality and cardiovascular disease (CVD). The prevalence of AOH increases with age, the presence of hypertension or diabetes and the use of antihypertensive or other medications. The implications of AOH for the treatment of CVD and hypertension are not well defined. This review provides an overview of the current information on this topic and recommends the more frequent assessment of OH in clinical practice and in future clinical trials.

Background: The pressor response to examination in the clinic setting is called the 'white coat effect' (WCE). This response may be a confounder when investigators use clinic blood pressure as a measure of response to antihypertensive therapy., Objective: ;To study the effect of the pressor response by evaluating the sex-specific effect of treatment with calcium antagonism on blood pressure measured in the clinic and by ambulatory blood pressure monitoring (ABPM)., Methods: Untreated hypertensive subjects (n=39) with seated clinic diastolic blood pressures (DBP) > or = 100 and < or = 130mmHg were studied. Same-day clinic systolic blood pressure (SBP) and ambulatory SBP were obtained after 1 week of placebo, and after 1 month of treatment with either nifedipine or verapamil in a randomized, blinded, parallel trial., Results: With placebo, women s average SBP was 18+/-;4mmHg lower than clinic SBP. By contrast, men s average SBP with placebo was 4+/-15mmHg lower than clinic SBP. There was a significantly greater reduction in clinic SBP for women than there was for men after 1 month of treatment (by 33+/-13 versus 18+/-18mmHg, P<0.005). However, reduction in ambulatory SBP after 1 month was the same for both sexes (20+/-11 versus 19+/-12mmHg)., Conclusions: In this study of moderate-to-severe hypertensives, the large WCE measured for women, which markedly diminished with treatment, accounts for the observed sex difference in response of clinic SBP to calcium antagonism. By contrast, with ABPM there was an equivalent response to treatment for both sexes. Use of ABPM could be a valuable means of eliminating the WCE as a confounder in clinical research.

Because left ventricular (LV) mass (LVM) is a powerful predictor of future cardiovascular events, it is important to identify hemodynamic and nonhemodynamic factors that increase LVM. We studied the separate contribution to LVM of daily arterial blood pressure (BP) and insulin resistance in a consecutive series of 29 (mean+/-SD age, 43+/-13 yr) nonobese (body mass index, 24+/-1.8 kg/m2), nondiabetic, glucose-tolerant subjects with untreated borderline or mild hypertension. The insulin sensitivity index (SI) was quantitatively determined from the frequently sampled iv glucose tolerance test. BP was characterized by ambulatory 24-h BP monitoring, and LVM index (LVMI) was determined by two-dimensional directed M-mode echocardiography. LVMI was directly related to 24-h mean BP (r=0.47; P=0.01). LMVI was also significantly related to Si (r=-0.43; P=0.02). In this nonobese group, neither LVMI nor Si was related to body mass index or age. After adjustment for the influence of BP on LVMI, a significant relation remained between LVMI and Si (P < 0.05). We conclude that in nonobese subjects with high normal BP, insulin sensitivity is related to LVM independently of BP and may be an important modulator of LV growth. In addition to a reduction of arterial BP, optimal prevention of LV hypertrophy in hypertensives may require improved insulin sensitivity.

Criteria for the diagnosis or exclusion of hypertension using ambulatory blood pressure monitoring have not been agreed upon. We designed this study to provide a statistically based guide for using results of ambulatory blood pressure monitoring to resolve this issue. To generate this information, we used a database of 228 subjects (135 men, 93 women; average age, 45 years) referred by their primary physicians over the past 7 years for evaluation of borderline or stage I hypertension (average blood pressure, 148/92 mm Hg; SD, +/-17.5/12.2 mm Hg). In this population, the pooled SDs of systolic and diastolic ambulatory blood pressures were 13.8 and 11.6 mm Hg, respectively. Using the pooled SD, we calculated the probability that a patient's blood pressure falls within the hypertensive range (> 140/90 mm Hg). The 95% confidence interval for each subject's blood pressure was also determined. For example, if 40 ambulatory blood pressure measurements are performed on a subject and the average systolic ambulatory blood pressure is 137 mm Hg, then there is a 10% probability that the patient's "true" average blood pressure is actually in the hypertensive range. By contrast, if the systolic pressure is 143 mm Hg, there is a 90% probability that the patient is hypertensive. This approach may be useful for clinical decision making and also for the design of clinical trials.

The purpose of this study was to assess several indexes of cardiovascular risk in men and women with moderate to severe hypertension. We found that women with moderate and severe hypertension have lower ambulatory blood pressure and less cardiac hypertrophy than men with similar clinic blood pressure.

Nifedipine gastrointestinal therapeutic system (GITS), a controlled-release delivery system given once a day, was evaluated in a multisite study of mild-to-moderate hypertensive subjects, seated diastolic pressure between 95 and 110 mm Hg, on placebo. Of 1,666 subjects enrolled, 69% were eligible to begin treatment. Therapy with nifedipine GITS was started at 30 mg daily and increased by 30 mg/day each week until there was a response (seated diastolic pressure < 90 mm Hg and a reduction of > or = 10 mm Hg) or until a maximum dose of 180 mg/day was reached. After titration, responders were kept on active treatment for 12 more weeks. Seventy-six percent of those treated responded, and 88% of the responders completed the 12-week phase. Comparisons were made among relevant subgroups. Elderly patients (age > or = 65 years) had a significantly higher response rate at a lower average daily dose, compared with younger subjects. Response rates were > 70% and relatively similar in (a) white and black patients, (b) diabetic and nondiabetic patients, (c) men and women, and (d) normal-weight, over-weight, and obese patients. Nifedipine GITS had no significant effect on fasting serum glucose or cholesterol fractions. Edema and headache were the most often observed adverse effects during treatment. Incidence of the former was related to dose but occurred without evidence of fluid retention (average body weight fell significantly by 1% during treatment). As antihypertensive monotherapy given once a day, nifedipine GITS is effective and well tolerated for a wide spectrum of hypertensive patients.

It has been hypothesized that insulin resistance and hyperinsulinemia contribute to the development of arterial hypertension. To further investigate this relationship, we compared arterial blood pressure in controls and women with polycystic ovary syndrome (PCO), an insulin-resistant state. Fourteen PCO women and 18 normal control women of similar age, body mass index, and race were studied. Plasma glucose and insulin levels were determined in an oral glucose tolerance test. The insulin sensitivity (SI) index was determined by the minimal model method. Systolic and diastolic blood pressure were measured by 24-h ambulatory monitoring. Left ventricular mass was assessed by echocardiography. The two groups had comparable fasting glucose levels, but the 2-h postload glucose was higher in PCO (8.0 +/- 0.5 vs. 5.6 +/- 0.3 mmol/L; P less than 0.001). Compared to controls, PCO women were significantly more insulin resistant by fasting insulin, 2-h insulin concentrations, and SI (28.3 +/- 6.7 vs. 68.3 +/- 10.0 min-1/nmol.mL; P less than 0.01). Average ambulatory systolic (121 +/- 2 vs. 118 +/- 2 mm Hg) and diastolic (76 +/- 2 vs. 73 +/- 2 mm Hg) blood pressures were similar for PCO and control women. No difference was found in left ventricular mass. Therefore, despite profound insulin resistance and hyperinsulinemia, women with PCO do not have increased arterial pressure or left ventricular mass.

Non-invasive ambulatory blood pressure monitoring was performed in a consecutive series of 87 subjects with recently detected mild uncomplicated hypertension. Obese subjects, diabetics and those with secondary hypertension were excluded. Ambulatory pressures were recorded on a day of usual activity. Average ambulatory systolic and diastolic pressures were significantly lower than referral pressures determined in clinics or screening sites and initial pressures taken by the monitors. Whereas men (57) and women (30) had similar referral and initial pressures, average ambulatory systolic pressure was significantly higher in men; diastolic pressure was not different. Men also had a significantly higher fraction of ambulatory systolic pressures greater than 140 mmHg compared to women. Fifty-six percent of the men and 80% of the women had average ambulatory systolic pressures less than 140 mmHg and diastolic pressures less than 90 mmHg; the difference between the sexes was significant (chi 2 = 6.99, P less than 0.01). Thus, in mild hypertension, women have lower average systolic pressure than men during ordinary daily activity. These results may account for lower long-term cardiovascular morbidity in hypertensive women compared with men.

Clinical data, arteriographic findings, peripheral and renal vein plasma renin activity (PRA) studies and responses to prostaglandin A1 infusion are presented from observations in seven hypertensive patients with renal artery stenosis. PGA1 infusion caused an increase in PRA and urine sodium excretion but no significant change in blood pressure. Exaggerated increases in PRA were observed in five patients. With cessation of PGA1 infusion PRA returned toward pre-infusion levels. In two patients bilateral renal and peripheral vein PRA's were determined before and during PGA1 infusion. PGA1 caused a greater increase in renal vein PRA than in peripheral vein PRA indicating a direct enhancement of renin secretion. These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis.

A single dose of guanabenz was examined for effects upon blood pressure, heart rate, plasma catecholamines, and plasma renin activity in a randomized, double-blind, crossover design. Eight patients were studied when supine, standing, and during submaximal exercise. Guanabenz reduced blood pressure in subjects who were supine or standing. Heart rate was lowered only in the supine subjects. Guanabenz induced reduction in plasma catecholamines subjects in all positions and the reduction correlated with the placebo level for both norepinephrine and epinephrine. Plasma renin activity was not significantly affected by guanabenz. The results indicate that the central alpha-agonist action of guanabenz reduces sympathoadrenal function to a greater extent in hyperadrenergic hypertensive patients than in those without this disorder.

The effect of selective glucocorticoid or mineralocorticoid replacement on pressor responses to angiotensin I and II and norepinephrine was studied in adrenalectomized rats given high salt intake. Four groups were prepared by 1) adrenalectomy only (n = 5); 2) adrenalectomy plus aldosterone, 6 micrograms/24 hr i.p. (n = 5); or 3) adrenalectomy plus dexamethasone, 10 micrograms/24 hr i.p. (n = 5), using miniosmotic pumps; and 4) sham adrenalectomy (controls; n = 5). Plasma corticosterone was undetectable in all three adrenalectomized groups. Plasma aldosterone concentration was similar in aldosterone-replaced and sham-operated controls. Pressor responses to various doses of angiotensin I, angiotensin II, and norepinephrine were determined in unanesthetized, undisturbed rats. Compared with both control and dexamethasone-replaced rats, pressor responses to all three agonists were significantly reduced in both nonreplaced adrenalectomized and aldosterone-replaced groups. Comparing the ratios of the pressor responses to angiotensin I and angiotensin II in the four groups over the entire dose range suggests that a greater fraction of injected angiotensin I was converted to angiotensin II in nonreplaced adrenalectomized rats than in the other three groups. We conclude that glucocorticoid action markedly contributes to the systemic pressor effect of angiotensin and norepinephrine. However, glucocorticoid deficiency does not impair in vivo conversion of angiotensin I to angiotensin II.

The effect of vasopressin infusion on the pressor dose responses to angiotensin II and norepinephrine was studied in pentobarbital-anesthetized and unanesthetized nephrectomized rats. Pressor vasopressin (2-15 ng X kg-1 X min-1) given to anesthetized rats decreased sensitivity to angiotensin II in a dose-dependent manner (r = 0.88), an effect completely reversible by dPMeTyrAVP, a vasopressin vascular antagonist. Subpressor vasopressin (0.5-1 ng X kg-1 X min-1) given to unanesthetized rats diminished sensitivity to angiotensin II in the presence or absence of pentolinium (10 mg/kg). Shifts in dose-response curves to angiotensin II were always parallel. In contrast, dose responses to norepinephrine were not modified by vasopressin in pentolinium-treated rats and showed a small nonparallel rightward shift in animals without pentolinium. In animals without pentolinium, the baroreflex-mediated reduction in heart rate elicited by angiotensin II was not altered by vasopressin infusion. Our data suggest that vasopressin reduces angiotensin II pressor action by diminishing pressor sensitivity to the peptide. They indicate that the effect may be specific, mediated through the vascular receptor for vasopressin and independent of actions of this hormone on the autonomic nervous system.

The separate role of mineralocorticoid and glucocorticoid hormone action in maintaining arterial pressure was studied in normotensive rats. Four groups were prepared: adrenalectomized (ADX) rats given 6 micrograms aldosterone/24 h (ALDO; n = 9) or 10 micrograms dexamethasone/24 h (DEX; n = 9) by intraperitoneal Alzet pumps, shamoperated controls (control; n = 10) and ADX rats with no hormone replacement (ADX; n = 9). All groups were given 1% NaCl + 2.5% glucose drinking solution. Measurements of plasma corticosterone and aldosterone and urinary aldosterone excretion confirmed the adequacy of the experimental groups. Forty-eight hours after ADX or sham, base-line intra-arterial mean arterial pressure (MAP) in conscious undisturbed rats was similar in the four groups. Captopril (1 mg/kg iv) produced a similar reduction in MAP in ALDO (-11 +/- 2 mmHg) and DEX (-12 +/- 1 mmHg) groups, despite a lower plasma renin activity (PRA) in ALDO (2.0 +/- 0.7 and 6.0 +/- 1.5 ng X ml-1 X h-1, respectively; P less than 0.05). dP (Me)TyrAVP (50 micrograms/kg iv) caused a greater decrease in MAP in ALDO (-15 +/- 3 mmHg) than in DEX (-8 +/- 1 mmHg; P less than 0.05). Combined blockade with both antagonists resulted in a greater MAP reduction in ALDO (-29 +/- 4 mmHg) than in DEX (-15 +/- 4 mmHg; P less than 0.05). These results indicate that glucocorticoid hormone action maintains arterial pressure in ADX rats by mechanisms similar to normal rats and largely independent of the renin-angiotensin system and vasopressin. In contrast, mineralocorticoid replacement alone in ADX rats requires increased participation of both peptide systems for maintenance of arterial pressure.

The effect of captopril was explored in salt-depleted methylprednisolone (MP)-hypertensive rats. MP treatment raised BP by 41+/-2 mmHg over 2 weeks. Controls (C) had no change in BP. Sodium balance and weight data indicated a greater salt depletion in MP than in C. On day 15, captopril reduced BP in both MP (20+/-4 mmHg) and C (31+/-4 mmHg). The effect was significantly smaller in MP than in C (p less than 0.05). Plasma renin activity (PRA) was similarly elevated in both groups, consistent with salt depletion. Serum (SCE) and lung-converting enzyme (LCE) activity were similar in MP and C. The diminished antihypertensive effect of captopril in MP is therefore not attributable to differences in PRA, SCE, or LCE. Our data suggest that depressor actions of captopril unrelated to the renin-angiotensin system are impaired in MP. Glucocorticoid-induced changes in vasodilator systems may explain these findings.

Participation of vasopressin and the renin-angiotensin system in the maintenance of systemic arterial pressure was evaluated in unanesthetized adrenalectomized rats. Adrenalectomized and sham-operated rats with implanted arterial and venous catheters were given 1% sodium chloride and 2.5% glucose as drinking fluid for 72 hours following adrenalectomy. Serum and urine samples were obtained for measurement of electrolyte and solute concentration. The pattern of serum electrolytes, serum osmolality, and renal excretion of electrolytes, solute, and water observed in the adrenalectomized rats was entirely consistent with previous observations in this model. Mean arterial pressure of unanesthetized unrestrained adrenalectomized rats was significantly lower than controls. In adrenalectomized rats, dPMeTyrAVP reduced mean arterial pressure 9 +/- 1 mm Hg, p less than 0.001; captopril then caused an additional reduction of 17 +/- 2 mm Hg, p less than 0.01. Neither antagonist altered arterial pressure in the control group. Our results indicate that vasopressin and the renin-angiotensin system play a compensatory pressor role in adrenal insufficiency, preventing a larger decrease of arterial pressure in this model of chronic hypotension.

The effect of methylprednisolone or deoxycorticosterone upon systemic arterial blood pressure and components of the renin-angiotensin system was studied in the rat. Rats maintained on regular diets given methylprednisolone suspension 20 mg/kg body wt demonstrated a significant increase in arterial pressure of + 37 plus or minus 5 mmHg, mean plus or minus SE, over a 2-wk period, whereas those treated with DOC and untreated controls showed no significant change. On normal diets, plasma renin concentration (PRC) of methylprednisolone-treated rats was significantly higher than that of DOC-treated rats. Methylprednisolone treatment also resulted in a significant elevation of plasma renin substrate concentration (PRS). Calculated plasma renin activity (PRA) was highest in methylprednisolone-treated rats, significantly above that of the DOC and no-steroid groups. NaCl supplementation resulted in a significant fall in PRC and PRA in all three groups; however, PRS remained significantly above normal in the methylprednisolone-treated rats. The pressor effect of angiotensin II was slightly increased in methylprednisolone-treated rats. Infusion of [Sar1,Ala8]angiotensin II (P-113) in methylprednisolone-treated rats resulted in a significant fall in diastolic arterial pressure. The results imply that methylprednisolone hypertension in the rat may be in part angiotensin dependent.

Arterial pressure and heart rate responses to intravenous infusions of epinephrine at rates of 4-64 ng/kg/min were determined in 15 healthy subjects. The state of physical conditioning in these subjects was assessed by resting (preinfusion) heart rate and bicycle ergometry. Predicted maximal oxygen consumption (pMVO2) was determined by performance at submaximal work loads. Significant correlations were observed between both preinfusion heart rate and pMVO2 and the threshold for the effect of epinephrine on systolic pressure, and the magnitude of the increase in systolic pressure. Neither preinfusion heart rate nor pMVO2 correlated significantly with the chronotropic effect of epinephrine (threshold or absolute increase in heart rate). The pMVO2 and preinfusion heart rate did not correlate significantly with preinfusion venous plasma epinephrine concentration or with plasma levels achieved during infusion. We conclude that physical conditioning increases the effect of circulating epinephrine on systolic arterial pressure without altering the chronotropic effect of this hormone.