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PubMed1996

High sodium sensitivity implicates nocturnal hypertension in essential hypertension.

We investigated the relationship between sodium sensitivity and diurnal variation of blood pressure in patients with essential hypertension. Twenty-eight inpatients with essential hypertension were maintained on high sodium (12 to 15 g NaCl per day) and low sodium (1 to 3 g NaCl per day) diets for 1 week each. Twenty-four-hour blood pressure and urinary sodium excretion were measured at the end of each diet period, and the sodium sensitivity index was calculated as the ratio of the change in mean arterial pressure to the change in urinary sodium excretion rate by sodium restriction. Patients whose average mean arterial pressure was lowered more than 10% by sodium restriction were assigned to the sodium-sensitive group (n = 16); the remaining patients, whose mean arterial pressure was lowered by less than 10%, were assigned to the non-sodium-sensitive group (n = 12). In the non-sodium-sensitive group, mean arterial pressure and heart rate fell during the nighttime, and average values of systolic, diastolic, and mean arterial pressures during the night were significantly lower than those during the day during both low and high sodium diets. On the other hand, in the sodium-sensitive group, there was no nocturnal fall in mean arterial pressure, and none of the systolic, diastolic, and mean arterial pressure values during the nighttime was different from the respective pressure values during the daytime during either sodium diet. The sodium sensitivity index was positively correlated with the fall in mean arterial pressure during the nighttime during a high sodium diet (r = .55, P < .01). These results indicate that in patients with sodium-sensitive essential hypertension, blood pressure fails to fall during the night. High sodium sensitivity may be a marker of greater risk of renal and cardiovascular complications, as has been found in nondippers, patients whose blood pressure fails to fall during the night.

Adult↗
PubMed2001

Development of genetic hypotheses in essential hypertension.

Essential hypertension illustrates the formidable task presented by the identification of genetic determinants of common disease. Making an initial genetic inference may prove difficult enough; the subsequent demonstration of functional significance at various levels of biological integration may be even more challenging. We review three instances in which an initial genetic inference has led to the development of testable hypotheses pursued at increasingly higher levels of biological organization. These include the adducin, the G protein beta3 subunit, and the angiotensinogen hypotheses.

Angiotensinogen↗
PubMedDate not supplied

Progress in cardiovascular diseases: cognitive function in essential hypertension.

Essential hypertension has rather recently become recognized as a major factor in the development of the 2 main types of dementia, that is, no longer merely vascular dementia but Alzheimer disease as well. The relationship between high blood pressure (BP) and the dementias is quite a complicated one, given a wide variability in temporal courses. The interval between the respective manifestations of hypertension and cognitive deterioration may vary from a few years to several decades. Moreover, temporal relationships may be obscured because of the observation that BP tends to fall in the face of imminent Alzheimer disease. Although the cause-and-effect sequence of this relationship has not been established, it may suggest that a low BP in this phase of life could be equally harmful as hypertension in the preceding period. Individual monitoring of BP and drug titration in the hypertensive elderly may well become mandatory in the highest age group. The question whether some antihypertensive drug categories might act more effectively in preventing cognitive deterioration than others, irrespective of their antihypertensive potential, remains. A modest meta-analysis on our part seems to suggest that suppression of the renin-angiotensin-aldosterone system (RAAS) would fail to offer such protection, in contrast to certain dihydropyridine (DHP) calcium-channel blockers. Unfortunately, recently published comparative prospective megatrials (Anti-hypertensive and Lipid-lowering Treatment to Prevent Heart Attack Trial and Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm) failed to carry any record on the mental status of the study populations, thereby missing a golden opportunity to resolve the above issue. Consequently, there remains an urgent need for further blinded long-term comparative hypertension trials, including follow-up evaluation of cognitive functions in relation to the course of BP.

Aged↗
PubMed2004

Genetics of essential hypertension.

Essential hypertension affects 1 billion people worldwide and its genetic basis is well established. For this review we surveyed the literature on the genetics of hypertension during the past 18 months and we now report the highlights. There has been publication of the two largest genome scans for blood pressure and new loci including significant linkage to chromosome 6q have been reported. The molecular basis of Gordon's syndrome has been partially unravelled with a dual function for WNK4 in ion transport regulation being discovered. There has also been progress in narrowing rodent quantitative trait loci using congenic approaches and several linkage peaks have now been demonstrated to have more than one loci. We also report some of the initial findings from pharmacogenetic studies.

Animals↗
PubMed1977

Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension.

Essential hypertension (EH) can be subdivided according to the sympathetic and renin activity into two contrasting forms: (1) borderline beta-hyperadrenergic renin hyperresponsive and (2) stable beta-hypoadrenergic renin hyporesponsive EH. These two forms probably represent two expreme poles in the spectrum of EH in which sympathetic and renin hyper- or hyporeactivity cannot be accounted for by catecholamine determinations solely. beta-Adrenergic responsiveness monitored by plasma cyclic AMP determinations revealed plasma cyclic AMP, renin and circulatory hyperresponsiveness to isoproterenol in borderline hyperadrenergic EH while the opposite, cyclic AMP and renin hyporesponsiveness to insulin-induced hypoglycemia have been described in low renin stable EH. The kidney is in the center of the adrenergic abnormality in the two forms of EH with the borderline one excreting into the urine catecholamines not accounted for by their glomerular filtration. Catecholamines solely, however, do not account for the differences in both forms of EH which can probably be attributed to their different beta-adrenergic responsiveness.

Adrenergic beta-Antagonists↗
PubMed1998

Ion channels in vascular smooth muscle: alterations in essential hypertension.

Essential hypertension is characterized by a near normal cardiac output but an increase in total peripheral resistance. In turn, total peripheral resistance is controlled directly by the diameter of the small arteries and arterioles like those in the kidney. The dynamic regulation of renal vessel diameter is governed by the contractile state of the vascular smooth muscle cells that line the vessel walls. This review addresses the role of a number of different ion channels to initiate and maintain the contractile state of the vascular smooth muscle cells in hypertension and the potential prevention of hypertension through gene therapy. These specific channels include Ca2+, K(Ca), Kv, and Cl- channels. In hypertension, it has been reported that increased activity of Ca2+ channels and decreased activity of Kv channels are responsible for the increased contractile tone and resting membrane potential observed in dissociated vascular smooth muscle cells from the spontaneously hypertensive rat. In contrast, increased activity of K(Ca) channels in vascular smooth muscle cells of the SHR has been hypothesized to dampen or brake the activity of Ca2+ and Kv channels. Finally, recent evidence suggests that introducing angiotensin II type-1 receptor antisense into prehypertensive rat pups prevents the onset of pathophysiological alterations observed in hypertension including K+ channel alterations. These results suggest that gene therapy may be a useful pharmacological and physiological tool to combat hypertension.

Animals↗
PubMed2003

Pathogenesis and consequences of essential hypertension.

Essential hypertension is a global problem with fairly high morbidity and mortality. The pathological mechanisms in hypertension are many and involve sympathetic nervous system, renin-angiotensin-aldersterone system, nitric oxide and a host of vasoactive substances. The consequences of hypertension are related either to hypertension or to atherosclerotic process in the arteries.

Humans↗
PubMed2006

[Susceptible genes of essential hypertension].

Essential hypertension (EH) is a complex multifactorial disorder with genetic and environmental factors contributing to its prevalence. The genetic features have been revealed from the significant familial aggregation and the consistency among twins. Therefore, identification of EH susceptibility genes will be helpful to understand the pathophysiology of the disease, identify populations with potential risks of developing the disease, and select antihypertensive drugs. The present article introduces the search strategies of EH susceptibility genes and some genetic variants related to EH; meanwhile, it tries to analyze the difficulties and the role for samples in identifying susceptibility genes to EH.

Genetic Predisposition to Disease↗
PubMed1993

Plasma lipids and platelet membrane fluidity in essential hypertension.

Essential hypertension is often associated with high levels of plasma cholesterol or triglycerides. The relationships between plasma lipids and platelet lipids, membrane fluidity and functions in untreated hypertensive patients were investigated by measuring the fluorescence anisotropies of two fluorescent dyes (DPH and its cationic derivative, TMA-DPH, with different subcellular localization), cytosolic Ca2+ and pH, cyclic AMP content and aggregation to ADP and collagen. Hypercholesterolemia was found to be accompanied by a rise in platelet cholesterol content without changes in TMA-DPH or DPH anisotropies whereas hypertriglyceridemia was associated with a decreased cholesterol to phospholipid molar ratio, a decreased DPH anisotropy and a tendency of the cytosol to alkalinize. These results point out the differences between the effects of an acute cholesterol load and those of chronic hypercholesterolemia on platelet membrane microviscosity and aggregation. They demonstrate a strong association between plasma triglyceride levels and platelet membrane structure.

Adult↗
PubMed2002

[The state of microcirculation in hypertensive disease (essential hypertension)].

Skin microcirculation was studied by laser doppler flowmetry in 149 patients with essential hypertension (92 men, 67 women; mean age 50.1+/-4.9 years) and in 25 normotensive controls. In patients with hypertension prevailed pathological hemodynamic types of microcirculation. Hyperemic, spastic and congestive types were found in 20.1, 23.5 and 40.3% of patients, respectively, while only 16.1% of patients had normal hemodynamic type. Moreover presence and severity of microcirculatory disorders depended on stage of hypertension and level of blood pressure. Thus, patients with essential hypertension had pronounced impairment of microcirculation caused by structural and functional changes of microcirculatory vascular bed.

Adult↗
PubMed1996

Hyperinsulinemia, family history of hypertension, and essential hypertension.

The aim of this study was the evaluation of the relationships among hyperinsulinemia, a family history of hypertension, and essential hypertension. Insulin and C-peptide responses to an oral glucose load were studied in 175 lean normotensives (N) and untreated hypertensives (H) with (F+) and without (F-) a family history of hypertension: 30 NF-, 30 NF+, 45 HF-, and 70 HF+. The groups were comparable for age, sex, body mass index, and blood pressure. The following parameters were evaluated: plasma glucose (G), serum insulin (I), and C-peptide (Cp) before and 30, 60, 90, and 120 min after the glucose load, fasting glucose/insulin ratio (ISI), fasting insulin/C-peptide ratio (I/Cp), and 24-h ambulatory blood pressure monitoring. Plasma glucose was measured, fasting and during the test, and it and I/Cp were similar in the four groups. Serum insulin and Cp, both fasting and stimulated, were significantly higher and ISI lower in normotensives and hypertensives with hypertensive parents. Grouping the subjects first on the basis of blood pressure and then on the basis of family history, no differences were found between normotensives and hypertensives, whereas I and Cp, fasting and stimulated, were significantly higher and ISI lower in subjects with positive as compared to negative family history. The closest correlations between insulin and ambulatory blood pressure were found in normotensive with hypertensive parents; in hypertensives with hypertensive parents we only found a direct correlation between fasting Cp and nocturnal blood pressure fall; in hypertensives with normotensive parents insulin inversely correlated with nocturnal blood pressure fall. Insulin resistance seems to have a familial basis, independently of the presence of hypertension. Instead of showing a causal relationship between insulin resistance and hypertension, our results indicate that the two are partly independent components of a common familial pattern.

Adult↗
PubMed1988

[Comparison of renal hemodynamics in 2 types of arterial hypertension, essential and renovascular, in man. Physiopathological implications].

Split renal function tests were studied in 41 patients with unilateral stenosis of the main renal artery in comparison with 36 subjects with essential hypertension. The two populations were matched for sex, age (39 +/- 10 vs 37 +/- 11 years (+/- 1 standard deviation) and systemic arterial pressure (193/114 +/- 29/15 vs 205/110 +/- 30/17 mmHg). The PAH clearance (CPAH) was decreased in essential hypertensives. The decrease was similar in the right (160.3 +/- 56.9 ml/min/m2) and left kidneys (158.7 +/- 45 ml/min/m2). The inulin clearance (Cin) was similar in both kidneys (35.2 +/- 12.5 vs 33.6 +/- 11.6 ml/min/m2). In addition, in essential hypertensive, CPAH was negatively correlated with blood pressure (p less than 0.01). In patients with renal artery stenosis, CPAH of the "stenotic" kidney was reduced (91.5 +/- 47.8 ml/min/m2) as well as Cin (22.9 +/- 9.3 ml/min/m2). In contrast, a significant increase in CPAH (194.1 +/- 63.8 ml/min/m2) and Cin (47.6 +/- 12.6 ml/min/m2) was observed in the contralateral kidney. Kidney function (CPAH and Cin) was not correlated with blood pressure in the "stenotic" kidney. CPAH and Cin of the non stenotic kidney were positively and significantly correlated with systemic arterial pressure (p less than 0.01). Cin was positively correlated with CPAH (p less than 0.001) in all kidneys in renovascular or in sustained essential hypertensives. However, in the contralateral kidney of renovascular hypertensives, a significant upward resetting of the correlation was observed. The Cin/CPAH was increased in the stenotic kidney (25.7 +/- 7.6%), as well as in the contralateral kidney (25.6 +/- 6.2%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Captopril and kidney function in renovascular and essential hypertension.

In the present study 25 patients with various forms of severe hypertension (essential hypertension: n = 12; renovascular hypertension: n = 11; unilateral small kidney: n = 2), which were treated with captopril for a mean control period of 34.9 months, were investigated. Reduction of mean blood pressure under captopril was comparable in all subgroups. However, patients with renovascular hypertension showed a significant increase in serum creatinine from 117 to 162 mumol/l (p less than 0.05) after 34.9 months, whereas in essential hypertensives even a slight decrease could be observed (113 vs. 111 mumol/l). Serum creatinine of the 2 patients with unilateral small kidney remained within the normal range. Changes in creatinine were markedly higher in cases with bilateral renal artery stenosis and/or in those with a very high initial plasma renin activity (greater than 15 ng/ml X 3 h). Our findings underline the necessity of cautious application of captopril in patients with renovascular hypertension.

Adult↗
PubMed1998

Vitamin C improves endothelium-dependent vasodilation by restoring nitric oxide activity in essential hypertension.

BACKGROUND: Essential hypertension is associated with impaired endothelium-dependent vasodilation. Inactivation of endothelium-derived nitric oxide by oxygen free radicals participates in endothelial dysfunction in experimental hypertension. To test this hypothesis in humans, we evaluated the effect of antioxidant vitamin C on endothelium-dependent responses in essential hypertensive patients. METHODS AND RESULTS: In 14 healthy subjects (47.1+/-4.8 years; blood pressure, 120.6+/-4.5/80.9+/-3.5 mm Hg) and 14 essential hypertensive patients (47.3+/-5.1 years; blood pressure, 153.9+/-7.1/102.3+/-4.1 mm Hg), we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 microg x 100 mL(-1) x min(-1)) or sodium nitroprusside (1, 2, and 4 microg/100 mL forearm tissue per minute), an endothelium-dependent and -independent vasodilator, respectively, in basal conditions and during infusion of intrabrachial vitamin C (2.4 mg/100 mL forearm tissue per minute). In hypertensive patients but not in control subjects, vitamin C increased (P<0.01) the impaired vasodilation to acetylcholine, whereas the response to sodium nitroprusside was unaffected. Moreover, in another 14 hypertensive patients (47.1+/-5.2 years; blood pressure, 155.2+/-6.9/103.7+/-4.5 mm Hg), the facilitating effect of vitamin C on vasodilation to acetylcholine was reversed by N(G)-monomethyl-L-arginine (100 microg/100 mL forearm tissue per minute), a nitric oxide synthase inhibitor, suggesting that in essential hypertension superoxide anions impair endothelium-dependent vasodilation by nitric oxide breakdown. Finally, because in adjunctive 7 hypertensive patients (47.8+/-6.1 years; blood pressure, 155.3+/-6.8/103.5+/-4.3 mm Hg), indomethacin (50 microg/100 mL forearm tissue per minute), a cyclooxygenase inhibitor, prevented the potentiating effect of vitamin C on vasodilation to acetylcholine, it is possible that in essential hypertension a main source of superoxide anions could be the cyclooxygenase pathway. CONCLUSIONS: In essential hypertensive patients, impaired endothelial vasodilation can be improved by the antioxidant vitamin C, an effect that can be reversed by the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine. These findings support the hypothesis that nitric oxide inactivation by oxygen free radicals contributes to endothelial dysfunction in essential hypertension.

Acetylcholine↗
PubMed2004

Hypothesis: Uric acid, nephron number, and the pathogenesis of essential hypertension.

BACKGROUND: Essential hypertension affects more than 25% of the world's population. Genetic, physiologic, and epidemiologic studies provide clues to its origins, but a clear understanding has been elusive. Recent experimental and clinical studies have implicated uric acid in the onset of essential hypertension. METHODS: In a retrospective chart review, we identified 95 children with confirmed, new onset hypertension, and evaluated the cause of hypertension and parental history of hypertension, birth weight, and serum uric acid. In an open-label, cross-over trial we treated 5 children with confirmed essential hypertension with allopurinol as single treatment agent, and screened for change in blood pressure by casual and ambulatory methods. In tissue culture experiments, we evaluated the effect of uric acid on glomerular endothelial cell function. RESULTS: Elevation of serum uric acid is related to the onset of essential hypertension in children, reduced birth weight, and endothelial dysfunction. Normalization of uric acid appears to ameliorate new onset essential hypertension. CONCLUSION: These findings, combined with animal model data, support the hypothesis that uric acid has a key role in the pathogenesis of early onset essential hypertension, and may unify some of the disparate theories of the origins of essential hypertension.

Animals↗
PubMedDate not supplied

Enalapril and enalapril-hydrochlorothiazide in the treatment of essential hypertension. The Enalapril-Hydrochlorothiazide in Essential Hypertension Canadian Working Group.

A total of 217 patients with essential hypertension were enrolled by 25 Canadian centers in this double-blind, parallel study to compare the efficacy and safety of enalapril administered alone or in combination with hydrochlorothiazide. After a 4-week placebo period, patients were given 10 mg of enalapril for 2 weeks. At the end of the 2 weeks of therapy, patients were maintained on the same dose of enalapril, titrated to a higher dose of enalapril, or received combination therapy with hydrochlorothiazide if their diastolic blood pressure remained > 90 mmHg. Patients in group 1 received enalapril 10 mg or 20 mg and those in group 2 received enalapril 10 mg alone or combined with hydrochlorothiazide 25 mg. The maintenance phase lasted 8 weeks. A standard mercury sphygmomanometer was used to measure blood pressure at each visit. The mean decrease in supine diastolic blood pressure (SDBP) was 16 mmHg in groups 1 and 2; the mean decrease in supine systolic blood pressure (SSBP) was 19 mmHg in group 1 and 20 mmHg in group 2. Eighty percent of the patients in group 1 and 81% of those in group 2 had an SDBP < or = 90 mmHg at the final visit. To achieve this control, 67% of the patients received enalapril 10 mg and 33% received enalapril 20 mg in group 1. In group 2, 70% of the patients received enalapril 10 mg and 30% received enalapril 10 mg plus hydrochlorothiazide 25 mg. Eighteen patients in group 1 and 17 patients in group 2 experienced one or more minor adverse events. The most frequently reported adverse events were headache, asthenia, abdominal pain, nausea, and dizziness. No major adverse events were observed. We conclude that enalapril used alone reduces blood pressure in the majority of patients with mild to moderate essential hypertension. When blood pressure is not controlled by enalapril alone, hydrochlorothiazide can safely be added to the regimen.

Adult↗