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 μg/kg/min, for one hour, and blood samples for renin determinations were drawn from the arterial cannula before and after infusion. Renin activity was measured by radioimmunoassay. At the termination of the SNP infusion, plasma renin activity had increased from 3.23±1.53 to 13.25±0.76 ng/ml/hr (P<0.05). Control animals that received only vehicle showed no change in renin activity. When rats that had received SNP at 40 μg/kg/min for one hour 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 μg/kg/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 μg/kg/min) resulted in elevations of renin activity to 22.50±0.90 and 19.84 ±1.94 ng/ml/hr, respectively. When saralasin was infused into rats receiving 160 μg/kg/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.
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine