Contribution of beta-adrenergic receptor mediated renin release to the maintenance of blood pressure during nitroprusside infusion in conscious rats.

The extent to which beta-adrenergic receptor mediated renin release contributes to the maintenance of blood pressure during hypotension induced by sodium nitroprusside (SNP, 40 micrograms/kg/min for 30 min) was assessed in conscious Wistar rats fitted with chronic aortic and vena caval catheters. Propranolol, (1.5 mg/kg, i.v.), reduced the basal level of plasma renin activity (PRA) in control rats from 4.4 +/- 0.4 to 2.4 +/- 0.4 ng angiotensin I/ml/min (p less than .05) and decreased PRA obtained during SNP infusion from 35.3 +/- 6.6 to 16.7 +/- 2.2 ng angiotensin I/ml/min (p less than .01). Despite the reduced PRA, the hypotensive response to SNP was not enhanced after propranolol. Treatment of these animals with captopril in order to block the actions of the remaining non-beta-receptor released renin, resulted in augmentation of the SNP hypotension. Captopril also potentiated SNP hypotension in rats that had not received propranolol. The addition of propranolol to the captopril treated rats produced no further change in SNP hypotension. The results of this study indicate that beta-receptor-mediated and beta-receptor-independent mechanisms contribute to the renin released during SNP hypotension. However, if the beta-receptor-mediated component alone is blocked, the remaining renin secretion is adequate to maintain blood pressure during SNP infusion.