Effect of Propranolol on Sodium Reabsorption and the Renal Circulation

Nomura, Gakuji; Arai, Shirõ; Uno, Denji; Shimao, M; Takata, Masanobu; Takabatake, Toshikazu; Hattori, Nobu

doi:10.1159/000172654

Cited by 3 publications

(3 citation statements)

References 5 publications

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“…Furthermore, acute administration of propran olol is reported not to change urinary sodium excretion [3] or even to induce an antinatriuretic effect in dogs [11], an increase in Na* excretion having been reported only in rats [12], In agreement with the animal find ings, intravenous administration of propranolol in man resulted in a decrease in renal plasma flow [13]. More generally, a deterioration in renal hemodynamics is at tributed to (3-blocker administration in man [2], with the exception of nadolol, for which an increase of renal plasma flow has been observed in animals and in man [3,4], The reduction of cardiac output is partly responsible for the decrease in renal hemodynamics associated with [3-blockers.…”

Section: Discussionmentioning

confidence: 97%

Renal Hemodynamic Effects of Tertatolol Compared with Those of Propranolol in the Conscious Dog

Laubie

Prost²,

Rochat³

1986

Am J Nephrol

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Experiments were performed in which the effects of two β-blockers, tertatolol [dl-(hydroxy-2’-t-butyl-amino-3’-propyloxy)-8-thiochroman hydrochloride] and propranolol, on mean arterial pressure (MAP), heart rate (HR), and renal function were studied in the conscious sodium-replete dog. In all experiments renal function was evaluated from the effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) assessed respectively by measurement of p-aminohippurate and creatinine clearances. These parameters were measured during two 30-min control periods, after which two further measurements were performed over a similar time period, after intravenous administration of either propranolol (0.5 mg·kg^-1; n = 8) or tertatolol (0.05 mg·kg^-1; n = 8), these two doses being of equivalent β-adrenoceptor antagonist activity. Administration of propranolol and tertatolol did not change MAP but induced a significant and comparable decrease in HR. After propranolol a significant decrease in ERPF was observed, without any change in GFR or sodium excretion. In contrast, administration of tertatolol resulted in no modification of ERPF, a slight but significant increase in GFR, and a significant increase in sodium and potassium excretion. These results suggest that tertatolol and propranolol though acting similarly on systemic parameters have different effects on renal hemodynamics in the conscious dog.

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Section: Discussionmentioning

confidence: 97%

Renal Hemodynamic Effects of Tertatolol Compared with Those of Propranolol in the Conscious Dog

Laubie

Prost²,

Rochat³

1986

Am J Nephrol

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“…This has been explained by the initiation of a reflex peripheral vasoconstriction (mediated by the sympathetic nervous system) in response to a reduced cardiac output following acute administration of these agents (Scriabine, 1979;Conway, 1980). In addition to their cardiac effects, some P-adrenoceptor blocking agents have been reported to reduce both renal blood flow and function, after acute administration, in both animals (Nies et al, 1971;Abdel-Razzak, 1977;Nomura et al, 1978) and man (Zech et al, 1975;Sullivan et al, 1976;Wilkinson, 1982). This renovascular effect may be a contributory factor in the increased vascular resistance seen with these agents.…”

Section: Discussionmentioning

confidence: 99%

“…The most consistent effects of a P-adrenoceptor blocking agent are to reduce cardiac output and heart rate (Nies et al, 1973;Garvey & Ram, 1975;Burden & Hamilton, 1976;Buckingham & Hamilton, 1980;Cohn, 1983). Although P-adrenoceptor blockade is not generally noted for any effects on renal function, it has been reported that P-adrenoceptor blocking agents can impair renal function, possibly through a reduction in renal blood flow, and an increase in Na'reabsorption (Nies et al, 1971;1973;Abdel-Razzak, 1977; Nomura et al, 1978). Clearly, the cardiac and renovascular responses to an ACE-inhibitor differ from those to a P-adrenoceptor blocking agent.…”

Section: Introductionmentioning

confidence: 99%

Cardiac and renovascular effects in the anaesthetized dog of BW A575C: a novel angiotensin converting enzyme inhibitor with β‐adrenoceptor blocking properties

Cambridge

Whiting

Allan

1988

British J Pharmacology

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1In the anaesthetized open-chest dog, BW A575C (N-(l-(S)-carboxy-5-[4(3-isopropylamino-2-(R,S)-hydroxypropoxy)indole-2-carboxamido]pentyl)-(R,S)-alanyl-(S)-proline) causes a dose-dependent inhibition of the isoprenaline response (increased cardiac rate). In this preparation BW A575C is approximately 50 times less active than propranolol, and 500 times less active than pindolol at the cardiac ,-adrenoceptor.2 At equieffective cardiac P,-adrenoceptor blocking doses in the anaesthetized, open-chest dog, BW A575C (5.0 mg kg-', i.v.) significantly reduces diastolic blood pressure and reduces cardiac contractility and rate. By contrast, propranolol (0.1 mg kg-', i.v.) and pindolol (0.01 mg kg-', i.v.) have little effect on diastolic blood pressure, but significantly reduce cardiac contractility and rate. The effects of BW A575C on cardiac rate are not significantly different from those of propranolol and pindolol, but its effects on cardiac contractility are significantly less than those of propranolol. BW A575C also produces some increase in left ventricular internal dimensions at end-diastole. This small cardiac dilatation is not significantly different from that observed with pindolol but is significantly less than that of propranolol. 3 In the anaesthetized closed-chest dog, BW A575C causes a dose-dependent inhibition of the angiotensin I pressor response. In this preparation BW A575C is approximately equiactive with enalapril at preventing the pressor response due to conversion of exogenous angiotensin I to angiotensin II (inhibition of angiotensin converting enzyme (ACE)). 4 At equieffective ACE-inhibition doses in the anaesthetized, closed-chest dog, BW A575C (1.0mg kg-' by i.v. infusion) significantly reduces diastolic blood pressure, cardiac contractility and rate, whereas enalapril (1.0 mg kg-' by i.v. infusion) only significantly reduces diastolic blood pressure.This blood pressure lowering effect ofenalapril is not significantly different from that of BW A575C. In this preparation BW A575C and enalapril also significantly increase renal blood flow, and renal excretion of urine and Na+. There is however no significant difference between their renovascular effects. 5 These studies demonstrate that BW A575C produces changes in cardiac and renovascular function which can be ascribed to its being an ACE-inhibitor and a P-adrenceptor blocking agent. The combination of these pharmacological properties results in a fall in blood pressure without compromising either cardiac performance or renal function.

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Comparative effects of propranolol and nadolol on renal blood flow in normal rats and rats with congestive heart failure

Brenner

Duchin

Ichikawa

et al. 1984

American Heart Journal

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Effect of Propranolol on Sodium Reabsorption and the Renal Circulation

Cited by 3 publications

References 5 publications

Renal Hemodynamic Effects of Tertatolol Compared with Those of Propranolol in the Conscious Dog

Renal Hemodynamic Effects of Tertatolol Compared with Those of Propranolol in the Conscious Dog

Cardiac and renovascular effects in the anaesthetized dog of BW A575C: a novel angiotensin converting enzyme inhibitor with β‐adrenoceptor blocking properties

Comparative effects of propranolol and nadolol on renal blood flow in normal rats and rats with congestive heart failure

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