Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of the frequency distribution of plasma-renin concentration in 81 patients with essential hypertension produced no evidence of a distinct sub-population with low renin levels. An arbitrary dividing line was used, therefore, to define low-renin hypertension (36% of patinets). Patients in this group were older than those with normal renin levels, and there was a significant negative correlation between renin and age among all patients. Low-renin hypertension was not characterized by increased exchangeable sodium, but exchaneable postassium was significantly lower than in patients with normal plasma-renin. This difference became insignificant when five patients in the low-renin group with persistent hypokalaemia were excluded. It is concluded that low-renin hypertension does not represent a separate diagnostic entity but that plasma-renin falls with age in essential hypertension.
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PMID:Is low-renin hypertension a stage in the development of essential hypertension or a diagnostic entity? 4 18

In a random sample of normotensive and hypertensive fifty-year-old men plasma-renin-activity (P.R.A.), plasma-renin-concentration (P.R.C.), and renin substrate were measured using radioimmunoassay for angiotensin I. P.R.A. in normotensives and untreated hypertensives were normally distributed with slight skewness to the right. The mean P.R.A. for untreated hypertensives (0.65 ng. per ml. per hour) was slightly, but not significantly, lower than that of the normotensive reference group (0.78 ng. per ml. per hour). Previously untreated hypertensives who had been off treatment for four weeks had either high or low P.R.A. depending on the previous treatment. No differences in the angiotensin-generation rate were noted as judged from the P.R.A./P.R.C. ratio. No differences in the renin-substrate concentration between the groups were found. The findings suggest that renin changes in essential hypertenion are secondary to pressure changes. Thus, the renin-angiotensin system may not be of primary pathogenetic importance in the development of essential hypertension.
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PMID:Renin-angiotensin system in essential hypertension. 5 Nov 45

Study of general haemodynamics in 15 patients with low-renin essential hypertension showed haemodynamic and pathophysiological heterogeneity. However, there was suppression of sympathetic nervous system function in all low-renin patients, regardless of haemodynamic pattern. Subnormal sympathetic nervous activity was manifested by a low normal mean plasma-noradrenaline concentration at rest, diminished noradrenaline responsiveness to postural stimulation, and a reduced blood-pressure response to the indirectly acting sympathomimetic amine tyramine. It is proposed that the syndrome of low-renin essential hypertension is of diverse aetiology, but with secondary sympathetic nervous system underactivity as a feature common to the various forms. The low plasma-renin activity is probably an expression of defective sympathetic nervous system stimulation of renin release.
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PMID:Suppression of sympathetic nervous function in low-renin essential hypertension. 5 83

The effects of timolol (10 mg thrice daily) and hydrochlorothiazide (50 mg/day) have been compared in a double-blind factorial trial in 20 patients with essential hypertension. There were four randomised test phases of 8 weeks each during which patients received timolol alone, hydrochlorothiazide alone, timolol plus hydrochlorothiazide, and no treatment (placebo). Blood-pressure was measured weekly, alternately at the outpatient clinic and at the patient's home. Supine mean arterial pressure fell from 119 mm Hg in the placebo phase to 110 mm Hg in the hydrochlorothiazide phase, 106 mm Hg in the timolol phase, and 101 mm Hg in the combined timolol plus hydrochlorothiazide phase. Factorial analysis revealed that these effects of the two drugs were additive without any potentiation or antagonism. Mean plasma-renin activity (P.R.A.) was 5-02 ng/ml/3 h in the placebo phase falling to 1-79 in the timolol phase and rising to 9-54 in the diuretic phase, but remaining unchanged in the combined treatment phase (5-40 ng/ml/3 h). The data suggest that the hypotensive action of timolol is not dependent on the concomitant fall in P.R.A. The methods described provide a valuable tool for quantitating the effects of a given drug, and hence a valid basis for objective comparison.
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PMID:Effects of timolol and hydrochlorothiazide on blood-pressure and plasma renin activity. Double-blind factorial trial. 6 May 66

In an attempt to resolve conflicting reports about the identity of a low-renin subgroup in essential hypertension, the distribution of plasma-renin activity (P.R.A.) has been examined in 82 hypertensive subjects before and after stimulation with bendrofluazide. The unstimulated basal P.R.A. showed no evidence of a separate subgroup of patients with low P.R.A. values although the distribution was slightly skewed with a tail to the right when compared with 83 normotensive subjects. In 38 of the patients post-stimulation P.R.A. observed in age and sex matched normotensive controls exposed to the same stimulus. However the percentage rise in P.R.A. in all 83 patients was less than half that of the controls. Thus the identification of a low-renin subgroup of hypertensive patients is critically determined by the standard of comparison employed: if the percentage rise is considered subnormal responsiveness is a feature of essential hypertension. If absolute post-stimulation values are used, there is a substantial group of patients with "low renin hypertension". The demarcation of such a group is, however, essentially arbitrary.
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PMID:Low renin hypertension. A distinct entity. 6 62

Inactive renin which can be converted to an enzymologically active form by acidification to pH 3-3 by dialysis was found in normal subjects and in patients with untreated essential hypertension. The molecular weight of this inactive renin (43 000) is 2000 +/- 900 (S.E.M.) daltons higher (p less than 0.05) than that of naturally occurring active renin and the two forms of renin could be clearly separated by ion-exchange chromatography with diethylaminoethyl-"Sepharose'. Patients with low-renin essential hypertension had proportionately larger amounts of inactive renin than usual, so that the total renin in these patients approached the normal range. Inactive renin seems likely to be a form in which the enzyme is secreted since in a patient with renal-artery stenosis its concentration was greater in the renal-vein blood coming from the affected kidney.
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PMID:An inactive higher-molecular-weight renin in normal subjects and hypertensive patients. 6 45

Human plasma contains renin, which is enzymatically active at neutral pH (active renin), and a non-dialysable factor, which has renin-like activity after treatment at low pH (inactive renin). In vitro activated plasma-renin and purified human renal renin showed identical enzyme-kinetic properties. Quantitative estimations of inactive renin in renal venous plasma from 5 patients with renal-artery stenosis demonstrated its release by the kidney. Acute stimulation of renin release by isoprenaline, tilting, or diazoxide in 13 normotensive individuals and in 9 patients with essential hypertension increased active plasma-renin and reduced inactive plasma-renin. Inactive plasma-renin was increased and active plasma-renin decreased during suppression of renin release by propranolol in 12 patients with essential hypertension. In 55 patients with various disorders, inactive and active plasma-renin were directly correlated. However, the concentration of inactive renin, for a given value of active renin, varied widely from patient to patient. These results indicate that so-called inactive renin is indeed physiologically related to active renin. They also suggest that inactive renin can be activated not only in vitro, but also in vivo. Different renin assays measure different relative amounts of active and inactive renin. This may call for reinterpretation of results obtained by various methods, especially in situations where changes in plasma concentrations of the two forms of renin are in opposite directions.
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PMID:Inactive renin in human plasma. 7 64

The angiotensin-blocking agent, saralasin, was given by rapid intravenous (bolus) injection to 21 hypertensive patients. A marked depressor response (average blood-pressure decrease of 30 mm Hg systolic and 20 mm Hg diastolic at 10 minutes after injection) was noted in 13 patients, of whom 11 had renovascular hypertension and 2 had high-renin essential hypertension. No change from prebolus blood-pressure was apparent at 10 minutes in 8 control patients with essential hypertension and normal or low peripheral plasma-renin activity. In all patients, blood-pressure response to saralasin bolus (10 mg) correlated with blood-pressure response to subsequent infusion of saralasin (10 microgram/kg/min). Blood-pressure response to rapid intravenous injection of saralasin--the "saralasin bolus test"--has many characteristics of an ideal screening procedure for renin-mediated hypertension.
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PMID:Saralasin bolus test. Rapid screening procedure for renin-mediated hypertension. 7 52

In normotensive subjects an inverse correlation was observed between an index of sympathetic nervous activity (the plasma-noradrenaline concentration during physical exercise) and reactivity to exogenous noradrenaline. This relationship was invariably disturbed in age-matched patients with essential hypertension. Multiple-regression analysis revealed a highly significant correlation between the combination of both factors and the height of mean arterial blood-pressure (r=0.91). The findings suggest that sympathetic nervous activity and pressor response to noradrenaline together form an important determinant of the arterial blood-pressure level. An inverse relationship could be demonstrated between plasma-renin concentration and pressor response to angiotensin II in normotensives, and this relationship was unchanged in hypertensive patients. Therefore angiotensin II does not appear to contribute directly to high blood-pressure.
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PMID:Sympathetic nervous system and blood-pressure control in essential hypertension. 8 87

The renal abnormality which causes hypertension in the Milan hypertensive strain of rats disappears as hypertension develops. Because of the many analogies between the condition in these rats and "essential" hypertension in man, the same pattern of change may occur if a renal abnormality is the cause of essential hypertension in man. This hypothesis was tested in two groups of young normotensive subjects matched for age, sex, and body-surface area; in the first group both parents were hypertensive, and in the second group both parents were normotensive. Renal plasma-flow, glomerular filtration-rate, plasma-volume, plasma-renin activity, plasma-concentrations of Na+, K+, and catecholamines, 24 h urinary excretion of Na+, K+, and aldosterone, and the cardiac index were measured so that renal function and the role of factors affecting blood-pressure regulation could be assessed. Renal plasma-flow was significantly higher (p less than 0.01) in the first group, whereas results of tests for all the other factors were almost the same in both groups. The hypothesis that a primary kidney abnormality causes hypertension in a proportion of patients with essential hypertension is proposed.
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PMID:A renal abnormality as a possible cause of "essential" hypertension. 8 3


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