Vasopressin in salt-induced hypertension of experimental renal insufficiency.

The purpose of these experiments was to determine if arginine vasopressin (AVP) contributes to the blood pressure elevation induced by salt excess in renal insufficiency. Conscious rats were studied 6 days after surgical removal of 85% renal mass, which resulted hi renal Insufficiency as evidenced by an elevation in BUN and creatlnine. Four groups of subtotally nephrectomized animals were studied; two at time zero and two following a 24-hour 0.9% NaCI Intravenous (l.v.) infusion. One group at each time had plasma AVP determined, while the other was given 30 ^g I.T. of a specific Inhibitor of the pressor effect of AVP. A fifth subtotally nephrectomized and a sixth normal nonsurgical group were observed without infusion for 24 hours, at which time plasma AVP was determined. Subtotal nephrectomy alone increased baseline BP and tended to increase plasma AVP levels over those of normal control animals. Twenty-four hour saline infusion increased BP in both infused groups by 29 ± 4 and 30 ± 3 mm Hg respectively. No change in BP occurred in either the subtotally nephrectomized or normal animals observed without infusion for 24 hours. Following saline infusion, BP decreased by 20.2 ± 1.5 in response to the AVP inhibitor as compared to 13 ± 1.5 mm Hg at time zero (p < 0.001). AVP was 42 ± 9.6 following saline infusion as compared to 10.5 ± 1.5 pg/ml at time zero (p < 0.001). Six of the saline-infused animals had urine collected over the 24 hours. The percent of Na excreted/Na infused was 83%, while the percent of volume excreted/volume infused was 91.5% (p < 0.05), demonstrating to an extent selective retention of Na as opposed to volume. Taken together, the elevation of plasma AVP and decrease in BP In response to AVP inhibitor in the saline-Infused animals demonstrate that AVP plays an important role in the BP elevation acutely induced by salt excess in renal insufficiency. (Hypertension 4 (suppl II): II-125-II-130, 1982)