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)

Acebutolol, a new cardioselective beta-blocking agent, was administered for 48 hours to 44 patients with essential hypertension at a total dosage of 2.0 g (2,000 mg). The slowing down of their pulse rate and the decrease in blood pressure were highly significant, whereas eight subjects treated with placebos had no change in either the pulse rate or blood pressure. Plasma renin activity decreased from 2.26 +/- 2.11 ng/ml/hour to 0.87 +/- 1.04 ng/ml/hour. The decrease in blood pressure was correlated with the initial plasma renin activity and with the decrease in plasma renin activity. These results demonstrate that a rapid decrease in blood pressure can be obtained in patients with essential hypertension treated with acebutolol and that the decrease in blood pressure is related to the initial state of the renin-angiotensin system.
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PMID:Rapid identification of patients with essential hypertension sensitive to acebutolol (a new cardioselective beta-blocker). 1 3

From analyses of the effectiveness of beta-blocker monotherapy in relation to the patient's age and to pre-treatment renin determinations an antihypertensive drug program is proposed in which beta-blockers form the cornerstone. Patients with essential hypertension can be subdivided into groups with low (19%), normal (59%), or high (23%) renin sodium index. The proportion with low renin hypertension increases with age. Patients with high renin fall into two categories: younger patients with fairly mild hypertension and older pateients with more severe hypertension and signs of renal disease. The antihypertensive efficacy of beta-blocker monotherapy is best in high renin forms, good but less consistent in normal renin patients and uniformly bad in low renin hypertensives. In relation to age, beta-blockers normalized blood pressure (larger than or equal to 95 mmHg diastolic) in three-quarters of the younger than 40-year-olds, in about half of those aged 40--60 years, but in only 20% of those aged over 60 years. On this basis, it is postulated that the older patients with a low renin exhibit a relatively hypoadrenergic state while those with a normal or high renin--for a given age and elevated pressure--have a relatively increased adrenergic nervous activity. Because the beta-blockers have a potent suppressive action on the renin-angiotensin system--and, as a consequence, on angiotensin vasoconstriction, aldosterone volume expansion and central stimulatory feedback mechanisms--their antihypertensive mode of action may be linked to an important extent, though not exclusively, to renin suppression.
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PMID:A beta-blocker-based antihypertensive drug program guided by age and renin. 1 22

Plasmin noradrenaline concentration after bicycle exercise (200 W for 2 min), compared with base line concentration, was used as an index of sympathetic responsiveness in patients with essential hypertension. Atenolol (JCI 66082, a "cardioselective" beta-blocker) was given in a daily dose of 200 mg to 16 patients for five weeks. This caused a decrease in supine blood pressure of 37/23 and, on standing, of 36/25 mm Hg compared with the placebo period. There was a significant correlation between the ratio of the increase in plasma noradrenaline concentration on exercise over its base line concentration and the subsequent fall in mean arterial pressure (r=0.840; P less than 0.001). There was a less significant correlation between plasma renin concentration and subsequent decrease in mean arterial pressure (r=0.542; P less than 0.05). Administrations of atenolol caused a rise in plasma noradrenaline both on lying and after exercise (P less than 0.0125), and a fall in plasma renin concentration (P less than 0.01). The results suggest that the antihypertensive effect of atenolol is related to the responsiveness of the sympathetic nervous sytem. Adrenergic activity is apparently an important determinant of blood pressure response to beta-blockade.
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PMID:[Sympathetic responsiveness and antihypertensive effect of beta-receptor blockade in essential hypertension: the effect of atenolol (author's transl)]. 1 16

Changes in blood pressure, plasma renin activity, and hemodynamic components were studied in 23 patients with essential hypertension treated with oral pindolol or propranolol. These beta-adrenergic blocking agents effectively lowered the blood pressure in the majority of the patients. Although plasma renin activity was not significantly changed, the higher was the pretreatment level, the more it tended to be decreased. Systemic vascular resistence was significantly decreased, while changes in cardiac index and circulating blood volume were variable. Pindolol showed less effect in reducing the heart rate than propranolol. The antihypertensive effect of these drugs had no correlation with the change in plasma renin activity or in any one of hemodynamic components.
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PMID:Effects of beta-adrenergic blocking agents on the blood pressure, plasma renin activity and hemodynamics of hypertensive patients. 1 42

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.
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PMID:Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension. 1 3

Several experimental observations accumulated during recent years have suggested an active participation of the sympathetic system in the pathogenesis and maintenance of hypertension in various experimental models of hypertension. The evaluation of sympathetic tone by various indirect means in human hypertension has also revealed that the sympathetic system plays an important role in the maintenance of hypertension in a subgroup of the human hypertensive population. The study of circulating catecholamines, which appears to be the best and most reliable indirect means to evaluate the sympathetic activity in the human, at present, has indicated that 25 to 40 per cent of patients with essential hypertension are characterized by higher basal circulating catecholamines and by a higher sympathetic reactivity in response to postural changes. These hyperadrenergic patients are also characterized by a higher heart rate, heart contractility, cardiac index and probably by higher plasma renin activity. The identification of these patients as a separate entity is desirable since it is possible that the evolution of the hypertensive disease and the response to therapy differ in this group of patients. The study of these patients could lead to a better understanding of the mechanisms underlying the pathogenesis of cardiovascular complications and to the development of more rational and efficient therapeutic approaches.
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PMID:The sympathetic system in hypertension. 2 13

The effect of beta adrenergic blocking agents on the renin release from the kidney and its possible role in the hypotensive effect of these agents were studied in patients with essential hypertension. Oxprenolol induced a significant decrease in systolic blood pressure and PRA, but the correlation between the decrease in blood pressure and the decrease in PRA was not found. When the effect of carteolol, another beta adrenergic blocking agent, was studied, a decrease in blood pressure was obtained, but there was a rise in PRA. These observations suggest that the hypotensive action of beta adrenergic blocking agents does not result from their effects on PRA.
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PMID:[The renin-aldosterone system in essential hypertension--hypotensive action of beta adrenergic blocking agents and variation of the renin-aldosterone system (author's transl)]. 2 66

The relationship between sympathetic responsiveness and the blood pressure reduction induced by long-term beta-blockade was assessed in patients with essential hypertension. The increase in plasma noradrenaline concentration during physical exercise was used as an index of sympathetic responsiveness. The cardioselective beta-blocker, atenolol, was given to 16 patients with sustained benign essential hypertension for five weeks at a dose of 200 mg/day. Atenolol induced a marked decrease in blood pressure and pulse rate during recumbency, orthostasis and exercise concomitant with a marked increase in plasma noradrenaline concentration (p less than 0.0125) and a pronounced decrease in plasma renin concentration (p less than 0.01). The ratio of plasma noradrenaline during exercise to the base line concentration correlated significantly with the subsequent decrease in mean arterial blood pressure induced by beta-blockade (r = 0.840; p less than 0.001). A less significant correlation was observed between the plasma renin concentration and the subsequent decrease in mean arterial pressure (r = 0.542; p less than 0.05). The results obtained indicate that sympathetic responsiveness is an important determinant of blood pressure response to beta-blockade induced by atenolol.
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PMID:Sympathetic responsiveness and antihypertensive effect of beta-receptor blockade in essential hypertension. 2 17

The changes in plasma renin activity (PRA) during short-term salt depletion (and peroral furosemide on the first day) and after bolus injection of propranolol were compared to the change during long-term treatment with diuretic and with propranolol in 19 patients with benign primary hypertension. A highly significant correlation was found between PRA on short-term and long-term salt depletion (r=0.02). A highly significant correlation was likewise found between initial PRA and decrement of PRA after bolus injection of or long-term treatment with propranolol. Only a weak inverse correlation was found between PRA reached during short-term salt depletion or long-term diuretic treatment and the fall in diastolic BP during long-term treatment (r=0.60). No significant correlation was found between decrease in PRA on propranolol (bolus/long-term) and diastolic BP reduction. It is concluded that the short-term PRA response to salt depletion and propranolol in the individual patient gives a good prediction of the PRA level on long-term diuretic or propranolol treatment, but is of no value in predicting the BP reduction during treatment.
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PMID:Acute and long-term salt depletion and beta-blockade: plasma renin activity response and its relation to blood pressure reduction in long-term treatment. 2 64

To investigate the initial potassium loss and development of hypokalaemia during the administration of an oral diuretic, metabolic balance studies were performed in ten patients with essential hypertension who had shown hypokalaemia under prior oral diuretic treatment. Chlorthalidone (50 mg daily) was given for 14 days. Six patients received a normal-sodium diet and four a low-sodium (17 mmol/day) diet. All patients had a normal initial total body potassium (40K). The electrolyte balances, weight, bromide space, plasma renin activity, and aldosterone secretion rate were measured. In both groups a potassium deficit developed, with proportionally larger losses from the extracellular than from the intracellular compartment. In the normal-sodium group the highest mean potassium deficit was 176 mmol on day 9, after which some potassium was regained; in the low-sodium group the highest deficit was 276 mmol on day 13. The normal-sodium group showed an immediate but temporary rise of the renin and aldosterone levels; in the low-sodium group renin and aldosterone increased more slowly but remained elevated. It is concluded that dietary sodium restriction increases diuretic-induced potassium loss, presumably by an increased activity of the renin-angiotensin-aldosterone system, while sodium delivery to the distal renal tubules remains sufficiently high to allow increased potassium secretion.
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PMID:Initial potassium loss and hypokalaemia during chlorthalidone administration in patients with essential hypertension: the influence of dietary sodium restriction. 2 52


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