Rebound hypertension after sodium nitroprusside-induced hypotension

Publisher Website
Google Scholar
Abstract
Patients undergoing surgical procedures using sodium nitroprusside-induced hypotension were studied to determine the role of the renin-angiotensin system in the pathogenesis of rebound hypertension (RH) after discontinuing sodium nitroprusside (SNP) infusion. Retrospective observations documented RH in 9 of 12 patients with a systolic blood pressure (SBP) increase from 112 .+-. 3.92 before SNP to 144 .+-. 5.60 torr 10 min after SNP (P < 0.001). In 12 patients, plasma renin activity (PRA) rose from 950 .+-. 432 to 3611 .+-. 1874 pg[picogram]/ml per h (P < 0.005) during SNP and remained elevated (2504 .+-. 792 pg/ml per h) 30 min after cessation of SNP. SBP rose from a control (pre-SNP) value of 112 .+-. 5.24 to 129 .+-. 8.52 torr after discontinuation of SNP (P < 0.05). Significant PRA and SBP changes did not occur in a matched group of patients who did not receive SNP. RH after cessation of SNP infusion was associated with persistent elevation of PRA. RH may be attributable to the unopposed effects of the renin-angiotensin system after the rapid plasma disappearance of SNP.