The Renin–Angiotensin System during Controlled Hypotension with Sodium Nitroprusside

Abstract

The role of the renin-angiotensin system in blood pressure homeostasis during sodium nitroprusside (SNP) infusion in the rat was evaluated. Rats received infusions of SNP, 40 .mu.g/kg per min, for 1 h and blood samples for renin determinations were drawn from the arterial cannula before and after infusion. Renin activity was measured by radioimmunoassay. At termination of SNP infusion, plasma renin activity had increased from 3.23 .+-. 1.53-13.25 .+-. 0.76 ng/ml per h. (P. < 0.05). Control animals that received only vehicle showed no change in renin activity. When rats that had received SNP at 40 .mu.g/kg per min for 1 h were treated with a competitive inhibitor of angiotensin II (saralasin), there was a 7-torr decrease in blood pressure (P < 0.01). Control animals showed no hypotensive response to saralasin. The hypotensive response to the administration of SNP at 40 .mu.g/kg per min in acutely nephrectomized rats exceeded that obtained in normal rats by 30 torr (P < 0.01). Enflurane anesthesia did not modify the renin response to SNP-induced hypotension. In conscious rats, larger doses of SNP (80 or 160 .mu.g/kg per min resulted in elevations of renin activity to 22.50 .+-. 0.90 and 19.84 .+-. 1.94 ng/ml per h, respectively. When saralasin was infused into rats receiving 160 .mu.g/kg per min, blood pressure decreased precipitously, and the rats died. SNP-induced hypotension stimulates renin release, and the subsequent production of angiotensin II helps maintain blood pressure.