AJP - Heart and Circulatory Physiology, Vol 258, Issue 4 994-1003, Copyright © 1990 by American Physiological Society

ARTICLES

Prevention of salt angiotensin II hypertension by servo control of body water

J. E. Krieger and A. W. Cowley Jr
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.

An automated servo-control system to maintain total body weight constant was used to investigate the role of fluid volume expansion in the development of salt-dependent hypertension in dogs continuously infused with subpressor doses of angiotensin II. Dogs maintained on a fixed salt and water intake were studied in metabolic scale cages, which enabled continuous 24 h/day monitoring of changes in body weight as an index of changes in total body water. Beat-by-beat hemodynamics were determined 24 h/day. Daily fluid and electrolyte balances and hormonal profile were determined. Blood volume was periodically measured by injection of 51Cr red blood cells. After a 3-day control period, salt intake was increased from 8 to 120 meq/day. In contrast to the rise of arterial pressure that was observed in our previous nonservo-controlled volume studies, average 24-h mean arterial pressure, cardiac output, and total peripheral resistance remained unchanged during a 4-day high-salt period. Total body weight was maintained within 7 +/- 17 g of the original weight. Blood volume was unchanged by day 2 as indicated by direct measurement (51Cr red blood cells) or by analysis of plasma protein concentration. There was a retention of 82 +/- 5 meq (P less than 0.05) of sodium on day 1 of high-salt period. Plasma sodium concentration increased approximately 7 meq/l (P less than 0.05) above control levels. Plasma renin activity and aldosterone decreased to undetectable values, whereas vasopressin and atrial natriuretic peptide increased significantly. These results confirm that elevations of blood volume and cardiac output normally observed when salt intake was increased in dogs infused with angiotensin II are secondary to water retention and that this salt-dependent model of hypertension is dependent on fluid volume expansion.

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