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.

Renin response and angiotensinogen control during graded hemorrhage and shock in the dog.

Hemorrhage and hemorrhagic hypotension have been shown to be potent stimulators of renin release. However, the relationship between angiotensinogen consumption and angiotensinogen production has yet to be completely defined during this type of circulatory stress. Peripheral renin activity increased progressively as the blood pressure was decreased stepwise by hemorrhage to 50 mmHg and remained elevated throughout the shock phase of the experiment. Angiotensinogen did not change from control (809 ng/ml) throughout hemorrhabic hypotension and shock. During hemorrhagic hypotension, with the infusion of the angiotensin antagonist, [1-sarcosine, 8-alanine]angiotensin II, angiotensinogen concentration fell progressively from 693 to 208 ng/ml at 50 mmHg. Intravenous angiotensin II infused continuously after the mean blood pressure reached 50 mmHg significantly elevated plasma angiotensinogen concentration. In conclusion, during hemorrhagic hypotension and shock, the kidney and the liver appeared capable of maintaining elevated plasma renin activity and adequate plasma renin substrate, angiotensinogen, respectively. The mechanism responsible for the maintenance of plasma angiotensinogen is suggested to involve a positive-feedback effect of angiotensin II on the liver.