Propranolol Inhibition of Renin Secretion

Fr, Bühler; Jh, Laragh; Baer, Leslie; Ed, Vaughan; Hr, Brunner

doi:10.1056/nejm197212142872401

Cited by 688 publications

(61 citation statements)

References 28 publications

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“…It is well established that propranolol prevents the rise in renin secretion caused by experimental adrenergic stimuli (3,5,12) and lowers PRA in hypertensive patients (13)(14)(15). In the present study, it was shown that oxprenolol, like d,l-propranolol, could prevent the rise in PRA caused by the beta adrenergic agonist, isoproterenol.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Effects on Renin Release of Beta Adrenergic Antagonists with Differing Properties

Weber¹,

Stokes²,

Gain³

1974

J. Clin. Invest.

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A B S T R A C T Continuous 6-h infusions of the beta adrenergic blockers dl-propranolol or oxprenolol significantly reduced plasma renin activity (PRA) and mean blood pressure in the resting rabbit and prevented the stimulatory effects of isoproterenol on renin release and heart rate. These actions were due to blockade of beta receptors, for the inactive isomer, d-propranolol, had no effect. Despite sustained high plasma concentrations of dl-propranolol (0.2 Ag/ml) in the unstimulated animal, PRA did not fall below 36% of control values, suggesting that basal renin secretion is maintained partly by factors other than beta adrenergic mechanisms.Prindolol, another beta blocker, also abolished the effects of isoproterenol on renin and on the heart, and reduced blood pressure in the resting animal. However, prindolol increased resting PRA and heart rate, and in animals already receiving dl-propranolol, it raised PRA and heart rate without further altering blood pressure. This suggests that the effect on PRA of prindolol was due to its intrinsic sympathomimetic activity and not hypotension-mediated mechanisms. The observation that the blood pressure-lowering effect of prindolol was associated with a rise in PRA, while another beta antagonist, H 35/25, lowered PRA but had no effect on blood pressure, indicates that the hypotensive action of beta blockers is unrelated to their effects on renin release.In both unstimulated and isoproterenol-challenged animals, only blockers possessing beta-i receptor affinity (d,t-propranolol, oxprenolol, prindolol, practolol, and metoprolol) affected heart rate, while effects on PRA were more prominent with agents possessing beta-2 activity (dl-propranolol, oxprenolol, prindolol, and H 35/25). Thus, the changes in PRA caused by the beta adrenergic blockers appear to be dependent upon the summation of their direct effects, antagonistic or sympathomimetic, on beta-2 adrenergic receptors regulating renin release.

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Section: Discussionmentioning

confidence: 99%

Comparison of the Effects on Renin Release of Beta Adrenergic Antagonists with Differing Properties

Weber¹,

Stokes²,

Gain³

1974

J. Clin. Invest.

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“…However, when we attempted to hybridise P-adrenoceptor blocking agents based on a benzene (atenolol like) or naphthalene (propranolol like) nucleus with an ACE inhibitor of the enalapril type the resultant compounds failed to exhibit dual activity (Allan et al, 1986a). However, we discovered that when the P-adrenoceptor blocking agent, pindolol and an ACE inhibitor of the enalapril type were used as templates for chemical hybridisation, the resultant chemical hybrid had dual activity (Allan et al, 1986b (Buhler et al, 1972;Case et al, 1978) it is quite clear that P-adrenoceptor blocking agents can exert hypotensive actions independent of this system e.g. direct effects on the heart and central actions (Prichard & Owens, 1986).…”

Section: Introductionmentioning

confidence: 99%

BW A575C, a chemically novel agent with angiotensin converting enzyme inhibitor and β‐adrenoceptor‐blocking properties

Allan

Cambridge

Hardy

et al. 1987

British J Pharmacology

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) is a chemically novel agent which exhibits in a single molecule both angiotensin converting enzyme (ACE) inhibition and P-adrenoceptor-blocking properties.2 BW A575C produced a competitive blockade of heart rate responses to isoprenaline in a guinea-pig right atrial preparation (pKB 7.18 ± 0.05, cf. pindolol 8.9 ± 0.7). BW A575C inhibited a partially purified preparation of ACE obtained from rabbit lung (IC50 10.7 + 2.1 nM, cf. enalaprilat, 4.4 ± 0.8 nM).3 Intravenous administration of BW A575C (1-100 tgkg-' min-')to the pithed rat inhibited in a dose-dependent fashion both angiotensin I-induced pressor responses and isoprenaline-induced tachycardia. Dose-ratios obtained from such studies demonstrated that, in this preparation, BW A575C was approximately 100 times more active as an ACE inhibitor than as a P-adrenoceptor blocking agent. 4 Intravenous administration of BW A575C (I mg kg-') to the conscious rat inhibited angiotensin Iinduced pressor responses, being approximately equipotent to enalapril and 10 times more potent than captopril. At the same dose, BW A575C had a similar duration of action as an ACE inhibitor to enalapril. 5 Intravenous administration of BW A575C (I mg kg-') to either conscious dogs or rats inhibited both angiotensin I-induced pressor responses and isoprenaline-induced heart rate responses. Doseratios obtained from such studies demonstrated that in these species, BW A575C was 2-10 times more active as an ACE inhibitor than as a P-adrenoceptor blocking agent.

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“…In this small study we were not able to relate the blood pressure response either to pre-treatment plasma renin levels or to the degree of suppression of renin during treatment, unlike Buhler, Laragh, Baer, Vaughan & Brunner (1973). This may be due to our failure to rigidly control dietary sodium intake before measuring PRA, but this is likely to be an almost universal practical problem (Woods, Pittman, Pulliam, Werk, Waider & Allen, 1976) and an absence of relationship of response to f1-adrenoceptor blockers to PRA has been reported by several groups (Leonetti, Mayer, Morganti, Terzoli, Zanchetti, Bianchetti, di Salle, Morselli & Chidsey, 1975;Epstein & Lubbe, 1977).…”

Section: Sodium and Potassiummentioning

confidence: 81%

A study of the effects of atenolol and propranolol on renal function in patients with essential hypertension.

Wilkinson¹,

Stevens²,

Pickering³

et al. 1980

Brit J Clinical Pharma

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1 The effects of propranolol and atenolol given in random order in a cross-over study to fifteen patients with essential hypertension have been studied. 2 Both drugs were effective in lowering blood pressure and side effects were not markedly different.3 There was no change in exchangeable sodium or potassium or in total body potassium during treatment with either drug. 4 Ambulant plasma renin activity was reduced by both drugs but the fall in blood pressure was not related to initial plasma renin. 5 Despite equal mean reduction in blood pressure with the two drugs, creatinine clearance fell significantly only during treatment with propranolol. 6 These observations suggest that intra-renal f2-adrenoceptors may be of importance in the regulation of renal function.

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Propranolol Inhibition of Renin Secretion

Cited by 688 publications

References 28 publications

Comparison of the Effects on Renin Release of Beta Adrenergic Antagonists with Differing Properties

Comparison of the Effects on Renin Release of Beta Adrenergic Antagonists with Differing Properties

BW A575C, a chemically novel agent with angiotensin converting enzyme inhibitor and β‐adrenoceptor‐blocking properties

A study of the effects of atenolol and propranolol on renal function in patients with essential hypertension.

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