Sympathetic Modulation of the Pressure-Dependent Renin Release in Conscious Dogs

Types of beta-adrenoceptors mediating renin release induced by isoproterenol were investigated in conscious dogs. The nonselective beta-adrenoceptor blocking drugs propranolol, D-32, and pindolol significantly inhibited increases in heart rate and plasma renin activity and a fall of blood pressure produced by intravenous infusion of isoproterenol (10 microgram . kg-1 . 20 min-1). d-Propranolol and d-D-32 did not inhibit these three responses to isoproterenol. The selective beta 1-adrenoceptor blocking drug atenolol, at the oral dose of 6 mg/kg, which selectively suppressed isoproterenol-induced tachycardia, significantly inhibited the renin release caused by isoproterenol. By contrast, the renin release induced by isoproterenol was not modified by the selective beta 2-adrenoceptor blocking drug IPS-339 at an oral dose of 3 mg/kg, which fully and selectively antagonized the fall of blood pressure in response to isoproterenol. There was good correlation between suppression of isoproterenol-induced renin release and that of isoproterenol-induced tachycardia after various beta-adrenoceptor blocking drugs. These results lead to the conclusion that in conscious dogs the beta-adrenoceptors mediating release are mainly of the beta 1 type.

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Pressure-Dependent Renin Release: The Kidney Factor in Long-Term Control of Arterial Blood Pressure in Conscious Dogs

Clinical and Experimental Hypertension Part A Theory and Practice ◽

10.3109/10641968709160173 ◽

1987 ◽

Vol 9 (sup1) ◽

pp. 181-195 ◽

Cited By ~ 5

Author(s):

H. Ehmke ◽

P. Persson ◽

H. Kirchheim

Keyword(s):

Blood Pressure ◽

Arterial Blood Pressure ◽

Conscious Dogs ◽

Renin Release ◽

Arterial Blood

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Effect of intrarenal administration of dopamine on renin release in conscious dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1983.244.1.h39 ◽

1983 ◽

Vol 244 (1) ◽

pp. H39-H45 ◽

Cited By ~ 1

Author(s):

H. Mizoguchi ◽

V. J. Dzau ◽

L. G. Siwek ◽

A. C. Barger

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Adrenergic Receptors ◽

Dose Range ◽

Plasma Renin ◽

Systemic Blood Pressure ◽

Conscious Dogs ◽

Renin Release ◽

Dopamine Antagonists ◽

Vasodilatory Action

We investigated the effect of intrarenal administration of dopamine on renin release in conscious dogs. Dopamine in doses ranging from 0.28 to 3.0 micrograms . kg(-1) . min(-1) produced a significant increase in systemic plasma renin activity (PRA) and renin secretion rate without altering systemic blood pressure. Dopamine also induced renal vasodilatation and natriuresis within this dose range. To determine if the dopamine-induced renin release is related to its vasodilatory action, two other vasodilators, papaverine and acetylcholine, were infused into the renal artery, but neither, in doses that produced a rise in renal blood flow similar to that of dopamine, had any effect on PRA. As dopamine can activate alpha- and beta-adrenergic receptors in addition to dopaminergic receptors, experiments were also performed to characterize the type of receptors involved in dopamine-induced renin release. Intrarenal infusion of sulpiride and haloperidol, dopamine antagonists, significantly inhibited dopamine-induced renin release and renal vasodilatation. In contrast, intrarenal infusion of propranolol failed to alter dopamine-induced rise in PRA or renal blood flow. Simultaneous infusion of phentolamine and dopamine, on the other hand, produced a significant potentiation of dopamine-induced renin release and renal vasodilatation. In conclusion, our studies demonstrate that dopamine is capable of inducing renin release and renal vasodilatation in conscious dogs. Moreover, such actions of dopamine are mediated through activation of specific dopamine receptors in the kidney. Finally, we present evidence for the existence of the intrarenal alpha-adrenergic mechanism that is inhibitory to renin release.

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Physiological concentrations of ANP exert a dual regulatory influence on renin release in conscious dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.263.3.r529 ◽

1992 ◽

Vol 263 (3) ◽

pp. R529-R536 ◽

Cited By ~ 1

Author(s):

H. Ehmke ◽

P. B. Persson ◽

A. Just ◽

B. Nafz ◽

M. Seyfarth ◽

...

Keyword(s):

Plasma Concentrations ◽

Renal Perfusion ◽

Conscious Dogs ◽

Renin Release ◽

Complete Suppression ◽

Control Mechanisms ◽

Response Curves ◽

Experimental Conditions ◽

Stimulus Response ◽

Extrarenal Renin

The influence of physiological increments in circulating atrial natriuretic peptide (ANP) on renin release was determined in conscious dogs. Renin stimulus-response curves (RSRCs) were obtained by controlled reductions of renal perfusion pressure (RPP) under control conditions and during intrarenal or intravenous ANP infusions. Under all experimental conditions, the RSRCs were characterized by a plateau, a threshold pressure (Pth), and a steep slope below Pth. Intrarenal ANP infusion (0.9 ng.kg-1.min-1), which induced a calculated threefold elevation of renal arterial ANP concentration (but did not change systemic arterial ANP levels), increased the slope of the RSRC by 81% (P less than 0.05) with no effect on Pth. A quantitatively similar effect on the slope of the RSRC (+90%; P less than 0.05) was observed when systemic ANP levels were raised (from 37 +/- 2 to 71 +/- 9 pg/ml; P less than 0.05) by intravenous infusions (3.6 ng.kg-1.min-1). In addition, however, intravenously infused ANP reduced Pth from 91 to 85 mmHg (P less than 0.05), which caused a complete suppression of the renin response to a reduction of RPP down to 85 mmHg. These findings indicate that ANP can inhibit renin release at physiological plasma concentrations by shifting the RSRC to a lower pressure level; this shift is mediated by a modulation of extrarenal renin control mechanisms. The direct effect of ANP on renin release is one of stimulation.

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