Beta-adrenergic control of renin in sodium-deprived conscious dogs: renal versus extrarenal location.
This study was designed to determine if tonic beta-adrenergic control of plasma renin activity (PRA) during dietary sodium restriction is due to stimulation of renal beta-adrenoceptors, extrarenal beta-adrenoceptors, or both. Experiments were performed in six conscious resting uninephrectomized dogs with chronically indwelling catheters in the aorta, vena cava, and remaining renal artery. The dogs were fed a low-sodium diet of approximately 7 mequiv. Na/day. PRA decreased by 28 +/- 4% of control (p < 0.01) when the beta-adrenoceptor antagonist propranolol was infused directly into the renal artery (ira) at a rate of 0.25 micrograms.kg-1.min-1 for 45 min, whereas iv propranolol infusion at the same rate had no effect on PRA. Propranolol infusion, 1 microgram.kg-1.min-1 iv, decreased PRA by 22 +/- 8% of control (p < 0.05) and produced significantly greater systemic beta-adrenoceptor blockade but a similar renal plasma propranolol concentration as with ira infusion, 0.25 micrograms.kg-1.min-1. Thus blockade of extrarenal beta-adrenoceptors produced no additional suppression of PRA beyond that which could be accounted for by blockade of renal beta-adrenoceptors. Therefore, suppression of PRA by propranolol is due solely to blockade of renal beta-adrenergic receptors in conscious sodium-deprived dogs.
Blair
M L
ML
Department of Physiology, University of Rochester School of Medicine, NY 14642, USA.
Gengo
F M
FM
D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004039:Diet, Sodium-Restricted; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D011433:Propranolol / Q000494:pharmacology*; D012083:Renin / Q000378:metabolism*; D013997:Time Factors
D011433:Propranolol; D012083:Renin