Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Haemodynamic and renin responses to dynamic exercise before and after intravenous beta-adrenoreceptor blockade with propranolol were compared in twenty-one patients with essential hypertension and either high (n = 7), normal (n = 7) or low plasma renin activity (n = 7). 2. Renin and heart-rate responses to exercise and beta-receptor blockade diminished from high-renin to normal and to low-renin patients, effects which were blunted with increasing age. 3. Among the renin groups cardiac output, stroke volume, diastolic pulmonary artery pressure, systemic pressure and peripheral vascular resistance as well as their changes produced by exercise and acute beta-receptor blockade were not significantly different. 4. Long-term anti-hypertensive propranolol effects correlated with pre-treatment renin status, renin stimulation and its suppression by acute beta-receptor blockade as well as with the exercise tachycardia and the patient's age. 5. The results suggest different adrenergic control mechanisms in renin sub-types of essential hypertension, age being a modulating factor.
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PMID:Haemodynamic responses to exercise and acute beta-receptor blockade in renin sub-types of essential hypertension. 107 70

Dopamine-beta-hydroxylase (DBH), the enzyme responsible for the biosynthesis of noradrenalin from dopamine, was assayed in the blood plasma of 20 men with primary hypertension. At the same time plasma was taken for measurement of plasma renin activity. Renin release as well as the plasma level of DBH is dependent upon the activity of the sympathetic nervous system, at least to some extent. A possible relationship between the two enzymes was therefore investigated. However, no relationship could be found in this series of 20 hypertensive patients. Another aim was to study the levels of DBH in venous and arterial blood simultaneously. No difference in the DBH level was found in venous and in arterial blood in 11 patients undergoing heart catheterization.
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PMID:Dopamine-beta-hydroxylase and plasma renin activity in twenty hypertensive subjects. 114 1

Acebutolol, a new cardioselective beta-blocking agent, has been given for 5 days, at a daily dosage of 600 mg to 8 patients with mild essential hypertension. Plasma Renin Activity (PRA), Plasma aldosterone (PA), Aldosterone Metabolic Clearance Rate (AMCR), Aldosterone Secretion Rate (ASR) have been compared before and after treatment. Whatever is the daily sodium intake, acebutolol decreases PRA and does not change AMCR. Under a normal sodium diet, PA and ASR are unchanged, in spite of the fall in PRA. On the contrary, under a sodium free diet, the decrease in PRA is accompanied by a decrease in PA and ASR.
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PMID:[Effects of acebutolol on the renin-aldosterone system in essential arterial hypertension]. 121 30

The acute renal, endocrine, and hemodynamic effects of the orally active endopeptidase inhibitor SCH 34826 (400 mg every 6 hours for five doses) were investigated in a group of 6 male patients [with established mild to moderate essential hypertension and left ventricular (LV) hypertrophy] in a balanced random-order double-blind, placebo-controlled cross-over study. Plasma atrial natriuretic factor (ANF) concentrations increased (p < 0.05) to fourfold control values after the first dose of inhibitor, but later postdose increments of ANF were less pronounced. Plasma cyclic GMP also increased significantly (p < 0.05). These effects were associated with a transient modest but significant (p < 0.05) increase in sodium excretion (50 mmol sodium in excess of placebo values) that was complete in 24 h. Mean 24-h urinary excretions of cyclic GMP and immunoreactive ANF were also significantly increased by 55 and 86%, respectively. Other urine indexes (including other electrolytes, volume, creatinine, aldosterone, and cortisol) and renal hemodynamics [including glomerular filtration rate (GFR) and effective renal plasma flow (RPF)] were unchanged. Renin-angiotensin-aldosterone system (RAAS) activity was not significantly altered. Plasma epinephrine increased after the initial three doses of SCH 34826. Systolic blood pressure (SBP) and heart rate (HR) were not altered by SCH 34826. Diastolic BP (DBP) increased slightly (p = 0.044). Acute inhibition of endopeptidase 24.11 by SCH 34826 in essential hypertension caused significant increments in plasma ANF and cyclic GMP together with modest natriuresis. No antihypertensive effect was observed in the first 30 h of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute inhibition of endopeptidase 24.11 in essential hypertension: SCH 34826 enhances atrial natriuretic peptide and natriuresis without lowering blood pressure. 128 Jul 35

These studies were undertaken to evaluate different manifestations of structural cardiovascular changes and the effects of antihypertensive therapy in essential hypertension. A meta-analysis of 109 studies that had examined the effect of different pharmacological blood pressure lowering regimens on left ventricular structure, examined by echocardiography, was undertaken to increase the statistical power, to resolve uncertainty and to improve the accuracy of estimation of the magnitude of effect. Strict preset criteria were applied. The effect of different drugs in monotherapy and in particular first line antihypertensive therapies were compared, using an analysis of covariance (ANCOVA). ACE-inhibitors, beta-blockers and calcium antagonists all reduced left ventricular mass (LVM) through a reduction in wall hypertrophy, the effect being most pronounced with ACE-inhibitors. Conversely, diuretics reduced LVM mainly through a reduction of left ventricular volume. Previously untreated males (n = 28, 86 kg, 46 years, 27 kg/m2) with non-malignant essential hypertension (supine diastolic blood pressure (DBP) > 95 mmHg 3-4 times (in triplicate) on placebo) were randomized to long-term double-blind treatment with enalapril (E) or hydrochlorothiazide (H). There were no significant differences between the groups at baseline. Vascular alterations in the retina (eyeground photo, refined grading), cardiac morphology (M-mode echocardiography, ASE), structural vascular changes of the hand (plethysmography, minimal resistance (Rmin)), total peripheral resistance ((TPR), calculated from dye-dilution) and blood pressure (intraarterial) were significantly interrelated at baseline except LVM and Rmin. After 6 months of therapy, E reduced the signs of vascular changes in the retina as well as Rmin in the hand circulation, while H did not change or increased these structural vascular changes. The blood pressure lowering effect of E (mainly through lowering of TPR) tended to be more pronounced, measured both intraarterially and indirectly, than that seen with H (mainly through lowering of cardiac output), however, there were no significant differences. LVM decreased progressively with E while the effect of H was non-significant. E reduced wall thickness but not left ventricular diameter and also improved left ventricular distensibility significantly. The effect on cardiac morphology was significantly different between therapies when taking change in blood pressure into account. After the longest follow-up on monotherapy (18 months) E had reduced LVM by 2.7 g/mmHg and H (14 months) by 1.3 g/mmHg (significant for E only). In univariate analysis the changes in cardiovascular structure were significantly related to the changes in the Renin-Angiotensin-Aldosterone System (RAAS).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Structural cardiovascular changes in essential hypertension. Studies on the effect of antihypertensive therapy. 134 61

1. Human renin gene restriction fragment length polymorphisms (RFLP) were compared in a Japanese family which has a high incidence of essential hypertension. 2. RFLP of human renin gene were observed in three restriction enzymes, Mbo I, Bgl I and Hind III; 1.4 kb and 1.0 kb [Mbo I], 5.0 kb and 9.0 kb [Bgl I] and 9.0 and 6.2 kb [Hind III]. 3. Plasma renin activity was not associated with blood pressure. 4. Renin gene RFLP were not cosegregated with essential hypertension in this Japanese family.
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PMID:Renin gene restriction fragment length polymorphisms in a Japanese family with a high incidence of essential hypertension. 135 34

The authors evaluated the assay performances and clinical usefulness of a newly developed solid phase radioimmunoassay (RIA) for total renin concentration (TRC) in human plasma. The direct total renin RIA was performed by a sandwich technique with a pair of anti-human renin monoclonal antibodies. Renin activation with trypsin did not change TRC. The RIA showed satisfactory assay performances and demonstrated full compatibility with a direct RIA-kit for active renin concentration (ARC) in human plasma. The values of TRC were 105.3 +/- 8.6 pg/mL in normal subjects and 136.5 +/- 14.6 pg/mL in patients with essential hypertension. The values of TRC and the ratios of ARC to TRC were high in patients with renovascular hypertension and were low in patients with primary aldosteronism. Although the TRC value in diabetic patients was 134.4 +/- 14.8 pg/mL, the ratio of ARC to TRC was low. The RIA procedure was simple since prior purification or activation of renin was not required. These results suggest that the total renin RIA and its combined use with the active renin RIA may be helpful in understanding the renin-angiotensin system in human plasma.
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PMID:Measurement of plasma total renin by the anti-human renin monoclonal antibodies. 177 17

Renin-angiotensin-aldosterone++ system was investigated in 60 patients suffering from rheumatoid arthritis. Forty-four of them (group 1) had arterial hypertension (144 +/- 4/94 +/- 2 mm Hg), sixteen were free of hypertension (120 +/- 3/80 +/- 1 mm Hg). Twenty-nine control subjects comparable by AH standing and demographic parameters had essential hypertension stage IB-IIA by A. L. Myasnikov classification (141 +/- 3/89 +/- 1 mm Hg). A tendency to renin suppression was dominating in 72% of group 1 patients (plasma renin activity less than 1.0 ng/ml/h). In this group there appeared high concentrations of A II (14.2 +/- 3.1 pg/ml) and plasma aldosterone++ (238 +/- 94 ng/ml). Rheumatoid vasculitis manifested in 86% of patients. Control subjects exhibited plasma renin activity greater than 3.0 ng/ml/hin 48%, average A II concentration was similar to that of group 1 (12.4 +/- 2.7 ng/ml/h, p greater than 0.05), plasma aldosterone++ level was significantly lower (176 +/- 29 ng/ml, p less than 0.05). Correlations were established between A II concentration and ESR (r = 0.39, p less than 0.05), A II and rheumatoid factor titers (r = 0.40, p less than 0.05). These indicate that immunopathological reactions are responsible for shifts in renin-angiotensin-aldosteron system in hypertensive rheumatoid arthritis subjects.
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PMID:[The renin-angiotensin-aldosterone system and arterial hypertension in patients with rheumatoid arthritis]. 187 68

A low dose of dopamine (1 microgram/min/kg) infused for 3 h, which is without systemic hemodynamic effects in normal subjects, increased the renal blood flow and renal production of prostacyclin (PGI2). This action was blocked by metoclopramide as well as by either of two cyclooxygenase (CO) blockers, but effects were not altered by administration of the alpha 1 blocker prazosin. Much of the effect of dopamine (DA) is apparently via the DA1 receptor, since fenoldopam (0.1 microgram/min/kg) reproduced these actions. However, although fenoldopam increased glomerular filtration rate and urinary Na+, CO blockers were without effect. In contrast neither DA or fenoldopam infusions changed either renal blood flow or PGI2 in a group of patients with essential hypertension. Renin secretion was shown to be increased via DA1 receptor activation both in humans and rat renal tissue. The DA2 receptor may also play a role since domperidone can reduce renal blood flow.
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PMID:Effect of dopamine on renal blood flow, prostaglandins, renin and electrolyte excretion in normal and hypertensive humans. 197 38

A prospective study was conducted to compare the frequency of renin gene polymorphisms in normotensive and hypertensive subjects. Hypertensive (n = 102, blood pressure 168 +/- 17/103 +/- 9 mm Hg) and normotensive (n = 120, blood pressure 122 +/- 10/75 +/- 9 mm Hg) subjects were white, had similar age and sex distributions (hypertensive group, 45 +/- 10 years old and 52% female; normotensive group, 44 +/- 9 years old and 55% female) and similar body mass index (hypertensive group, 23.2 +/- 2.6; normotensive group, 22.5 +/- 2.4 kg/m2, p = 0.048). The familial susceptibility to hypertension was defined as at least one parent and one sibling who were hypertensive before age 65; subjects in the normotensive group had no familial history of hypertension. Renin gene polymorphisms located throughout the renin gene were identified by using three restriction enzymes (Taq I, HinfI, HindIII). For each polymorphic restriction site, allele frequencies were similar in the hypertensive and the normotensive groups. In the absence of parental genotypes, the haplotype frequencies combining the three restriction fragment length polymorphisms were estimated by using maximum likelihood techniques and were similar in both groups (hypertensive group, 0.429, 0.277, and 0.177; normotensive group, 0.453, 0.245, and 0.195 for the three most common haplotypes). A rare haplotype detected by Taq I/Hind III was apparently more frequent in the hypertensive than in the normotensive group (hypertensive group, tH 0.086, th 0.022; normotensive group, tH 0.038, th 0.050), but the difference was not statistically significant. In conclusion, no association between renin gene polymorphisms and essential hypertension was demonstrated in the present study.
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PMID:Similar frequencies of renin gene restriction fragment length polymorphisms in hypertensive and normotensive subjects. 197 31


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