β-Adrenergic control of renin in sodium-deprived conscious dogs: renal versus extrarenal location

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Abstract
This study was designed to determine if tonic β-adrenergic control of plasma renin activity (PRA) during dietary sodium restriction is due to stimulation of renal β-adrenoceptors, extrarenal β-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 β-adrenoceptor antagonist propranolol was infused directly into the renal artery (ira) at a rate of 0.25 μg ∙ kg−1 ∙ min−1 for 45 min, whereas iv propranolol infusion at the same rate had no effect on PRA. Propranolol infusion, 1 μg ∙ kg−1 ∙ min−1 iv, decreased PRA by 22 ± 8% of control (p < 0.05) and produced significantly greater systemic β-adrenoceptor blockade but a similar renal plasma propranolol concentration as with ira infusion, 0.25 μg ∙ kg−1 ∙ min−1. Thus blockade of extrarenal β-adrenoceptors produced no additional suppression of PRA beyond that which could be accounted for by blockade of renal β-adrenoceptors. Therefore, suppression of PRA by propranolol is due solely to blockade of renal β-adrenergic receptors in conscious sodium-deprived dogs.Key words: propranolol, sympathetic nervous system, plasma renin activity, dietary sodium restriction.