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.