Action of angiotensin II on renal blood flow and function during hemorrhagic shock.

The purpose of this study was to evaluate during hemorrhagic hypotension and shock the effect of angiotensin II on renal blood flow, glomerular filtration rate, and sodium and potassium excretions, and to determine its role in the development of irreversible hemorrhagic shock. Anesthetized dogs were subjected to a hemorrhagic shock protocol. Angiotensin II was infused at 100 ng/kg/min i.v. from 50 mm Hg initial hemorrhage until the experiment was terminated. The survival time from 50 mm Hg initial hemorrhage to reinfusion was increased significantly from 2.7 +/- 0.5 h to 4.7 +/- 0.8 h by exogenous angiotensin II. However, once shock had developed, the survival time from reinfusion to 50 mm Hg normovolemic hemorrhagic shock was not affected by exogenous angiotensin II (4.4 +/- 1.4 to 3.6 +/- 0.7 h.) During hemorrhagic shock, exogenous angiotensin II significantly increased sodium excretion and total renal blood flow. Glomerular filtration rate, potassium excretion, and arterial sodium and potassium concentrations were not affected. These data indicate that angiotensin II prolonged the development of irreversible hemorrhagic shock and selectively increased sodium excretion and total renal blood flow.