ENDOGENOUS ANGIOTENSIN STIMULATION OF VASOPRESSIN (AVP) IN THE NEWBORN LAMB

Abstract

Exogenous renin or anglotensin II (A II) infused peripherally or into the CNS will stimulate thirst and AVP release. Whether the endogenous renin-anglotensin system physiologically stimulates thirst or AVP secretion is unknown. To assess the effect of endogenous renin-angiotensin stimulation on AVP secretion in the lamb, nine normal newborn lambs were stimulated with furosemide (FU) 2 mg/kg infused I.V. alone, and with the A II inhibitor 1-sar, 8-ala, A II, 5 μg/kg/min. Six anephric lambs received only FU. Blood samples were drawn at 8, 20, 35, 65 and 125 min. post infusion. PRA (ng/ml/hr), aldosterone (aldo, ng/dl) and AVP (μU/ml) were measured by RIA. (M and SEM) PRA increased within 8 min. from a baseline of 16.7±5.0 to 30.2±12.3 (p<.05), and remained elevated through 120 min. Plasma Aldo and AVP increased post FU from respective baselines of 14.2±4.7 and 2.7±0.,5, to 28.5±13.2 and 9.9±3.5 at 35 min. (p<.05), and thirst-like behavior was observed. AVP, thirst, and Aldo did not increase after FU in anephric lambs or in normal lambs treated with A II inhibitor. There were no changes in mean plasma sodium, Hct, or osmolality, and minimal changes in systemic blood pressure and plasma protein concentration during the first 35 min, after FU. We conclude: 1) that FU stimulates Aldo, AVP and thirst via direct renal stimulation of renin, 2) the Aldo, AVP and thirst responses to FU are mediated by A II release and 3) these responses all are intact in the newborn period.