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)

Beta adrenergic receptor antagonists (beta blockers) differ greatly in their cardioselectivity and intrinsic sympathomimetic activity, and these differences may have important therapeutic consequences. We have therefore studied the effect on blood pressure, heart rate and plasma renin activity of the beta blocking drug oxprenolol (Trasicor) which has considerable intrinsic sympathomimetic activity, both alone and in combination with the benzothiadiazine cyclopenthiazide. Eleven patients with mild to moderate benign essential hypertension were randomly allocated to one of two treatment groups. Oxprenolol was given as the first drug to Group 1, and cyclopenthiazide as the first drug to Group 2. The patients were assessed before the start of treatment, after 2 to 3 weeks of treatment with one drug and after a further 2 to 3 weeks of treatment with both drugs. Heart rate, blood pressure and plasma renin activity were measured with the patients recumbent and after a standardized tilt to 85 degrees to provide a reflection of day to day cardiovascular stress. Oxprenolol reduced arterial blood pressure without inducing significant bradycardia. The addition of cyclopenthiazide had little further effect. Oxprenolol alone suppressed plasma renin activity both at rest and during tilt and also abolished the increase in plasma renin activity after administration of cyclopenthiazide. The combination of (1) moderate reduction of blood pressure. (2) inhibition of the otherwise inevitable increase in plasma renin activity with the use of a diuretic drug, and (3) only moderate inhibition of overall sympathetic activity indicates that it is possible to achieve physiologic balance with the appropriate beta blocking drug.
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PMID:Beta adrenergic blockade and diuretic therapy in benign essential hypertension: A dynamic assessment. 0 63

Studies in 55 patients with benign essential hypertension showed that the beta-blockers bufuralol (22 patients) and propranolol (33 patients) at a dose ratio of 1:4, possess comparable antihypertensive efficacy despite different properties regarding intrinsic sympathomimetic activity. Beta-blocker-monotherapy normalized blood pressure ( less than 140/90 mm Hg) in one fourth of the patients. Body weight and plasma and blood volumes remained unchanged during beta-blockade of four to six weeks duration, the mean plasma potassium was slightly increased. The inhibition of plasma renin activity (PRA) was more pronounced with propranolol (-69%) than with bufuralol (-47%). Wirth both beta-blockers decreases in blood pressure correlated inversely with pre-treatment PRA (p less than 0.05). Propranolol-induced changes in blood pressure correlated also with associated changes in PRA (p less than 0.005); in contrast, no such relationship was observed with bufuralol. The blood pressure effects of bufuralol, however, correlated significantly with changes in urinary noradrenaline excretion (r=0.41; p less than 0.05). Patient sub-groups with low, normal or high pre-treatment PRA in the average showed a comparable pattern of pre-treatment noradrenaline excretion and patients with normal renin levels exreted more adrenaline than those with low renin levels (p less than 0.001). These data are consistent with the concept that in untreated essential hypertension PRA may be an index of adrenergic activiity, the latter representing an important determinant of blood pressure response to beta-blockade. The blood pressure lowering effects of bufuralol in benign essential hypertension seem to be independent of renin and may be related, at least partly, to diminished free peripheral noradrenaline levels.
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PMID:[Interrelations between blood pressure, blood volume, plasma renin and urinary catecholamines during beta-blockade in essential hypertension (author's transl)]. 0 63

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

Two beta-blocking agents with different properties were used to define the adrenergic component of the renin release which follows orthostasis. Five normal young subjects were tilted to 85 degrees for 30 min on four separate occasions. In two control studies the release of renin, as indicated by changes in plasma-renin activity, was highly reproducible. The effects of intravenous oxprenolol and intravenous propranolol, were then compared under the same experimental conditions. Oxprenolol attenuated the renin response in all subjects without completely abolishing it. Propranolol completely abolished the renin response. The difference in the ability of these agents to suppress renin release may be related to the presence (oxprenolol) or absence (propranolol) of intrinsic sympathomimetic activity. The increased rate of renin release in orthostasis seems to be mediated entirely by the adrenergic nervous system.
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PMID:Is the adrenergic control of renin release dominant in man? 6 40

Preexisting increase of plasma renin activity in hypertension seems to indicate an effective hypotensive action of adrenergic beta-receptor antagonists. In spite of marked elevation of plasma renin activity in Goldblatt-rats, the beta-blocker Pindolol failed to lower the blood pressure. On the contrary, high doses of this substance led to an acceleration of the Goldblatt-type hypertension, perhaps because of the intrinsic sympathomimetic activity of Pindolol. These findings support the conception that beta-blockers are effective in lowering the blood pressure only in hypertension with stimulated renin secretion, which is caused by an increased activity of the sympathetic nervous system. Plasma renin activity was not altered by Pindolol. There existed a linear relationship between blood pressure and left-ventricular weight in all groups of rats, which was not impaired by Pindolol in all used doses.
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PMID:[The influence of the beta-blocking agent pindolol on blood pressure and heart weight of rats with Goldblatt-type hypertension (author's transl)]. 14 Feb 70

The importance of the sympatho-adrenal system for the isoprenaline-induced increase in plasma renin concentration was investigated in conscious rats Ganglionic blockade by trimethidinium (10 mg kg-1) increased the dose-dependent elevation of plasma renin concentration induced by isoprenaline (0.03-0.48 microgram kg-1 min-1). Also treatment of the rats with guanethidine (6 mg kg-1) or reserpine (2.5 mg kg-1, given 16 and 7 h prior to the experiments) further increased the effect of isoprenaline (0.5 microgram kg-1 min-1) on plasma renin concentration. Unilateral renal denervation combined with contralateral nephrectomy doubled the effect of the beta-sympathomimetic amine on renin release. The alpha-adrenoceptor antagonist phenoxy-benzamine (3 mg kg-1) also enhanced the effect of isoprenaline on this parameter. It is concluded that apart from a stimulation of renin release via beta-adrenoceptors the sympathetic nervous system may inhibit renin release via stimulation of alpha-adrenoceptors.
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PMID:alpha-Adrenoceptor-mediated inhibitory effect of the sympathetic nervous system on the isoprenaline-induced increase in plasma renin concentration. 19 79

The beta-sympathomimetic amine isoprenaline increases the plasma renin concentration by a stimulation of beta-receptors which control renin release. Isoprenaline also lowers systemic blood pressure and causes a reflex-mediated activation of the sympathetic nervous system. In these investigations it has been tested to see whether the catecholamines released by this activation modulate renin release by stimulation of certain alpha-receptors. Pretreatment of rats with reserpine or with the ganglionic blocking agent Trimethidinium enhanced the increase in plasma renin concentration induced by isoprenaline. So did pretreatment with the irreversible alpha-receptor antagonist phenoxybenzamine. Renal denervation also increased the effect of isoprenaline on plasma renin concentration. It is concluded that catecholamines released from the sympathetic nervous system can decrease renin secretion by an activation of certain alpha-receptors. The sympathetic nervous system may thus exert control of renin release by beta-receptors which stimulate and by alpha-receptors which diminish renin secretion.
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PMID:[Double controlled regulation of renin release by the sympathetic nervous system. Stimulation via beta receptors and inhibition via alpha receptors]. 19 32

The beta-adrenoceptor antagonists, atenolol, metoprolol and propranolol, administered intravenously to anaesthetized rats in doses producing equal beta1-adrenoceptor blocking effects, caused comparable suppression of plasma renin activity (PRA) despite the fact that, at these doses, atenolol and metoprolol exhibited no beta2-adrenoceptor blocking properties. Practolol, an agent specific for beta1-adrenoceptors but possessing intrinsic sympathomimetic activity, caused less marked suppression of PRA. When doses of atenolol, metoprolol, propranolol and butoxamine were selected to achieve equal beta2-blocking effects, PRA was again significantly suppressed by atenolol and metoprolol but not by propranolol or butoxamine. These results do not support the concept that adrenergic release of renin is mediated by beta2-adrenoceptors, but are compatible with the involvement of a beta1-adrenoceptor-mediated mechanism.
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PMID:The beta-adrenoceptor controlling renin release. 21 37

The effect of the indirect sympathomimetic agent tyramine on the isoprenaline-induced increase in plasma renin concentration was investigated in conscious rats. Tyramine caused a dose-dependent decrease in the isoprenaline-induced elevation of plasma renin concentration. Pretreatment of the rats with reserpine abolished this effect of tyramine, indicating that tyramine released catecholamines which acted on the inhibitory adrenoceptors. Pretreatment with phenoxybenzamine, an alpha-adrenoceptor antagonist, also abolished the inhibitory effect of tyramine on renin release, indicating that alpha-adrenoceptors mediated the observed inhibition of renin release. In rats with chronically denervated kidneys tyramine did not inhibit renin release. It is concluded that catecholamines which are released from renal sympathetic nerve endings can suppress renin release by activating alpha-adrenoceptors.
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PMID:Inhibitory effect of tyramine-induced release of catecholamines on renin secretion. 67 21

The vasoconstrictors angiotensin II, vasopressin and the alpha-sympathomimetic phenylephrine significantly inhibit the renin release caused by the beta-sympathomimetic isoprenaline. The mechanism of the inhibition is discussed.
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PMID:Inhibition of isoprenaline-induced increase in plasma renin concentration by vasoconstrictors. 117 48


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