Circulation Research, Vol 39, 788-797, Copyright © 1976 by American Heart Association

ARTICLES

Acute and chronic dose-response relationships for angiotensin, aldosterone, and arterial pressure at varying levels of sodium intake

AW Cowley and RE McCaa

We examined the acute and chronic dose-response relationships between intravenously infused angiotensin II (A II) and the resulting changes in arterial pressure and plasma aldosterone concentration at varying levels of sodium intake. Sequential analysis of plasma aldosterone at each A II infusion rate resulted in an acute dose-related increase in plasma aldosterone which was markedly attenuated after the first 24 hours of infusion, the final level being directly related to the dose of A II and inversely related to sodium intake. A II infused at 5,15, and 23 ng/kg per min was associated with an initial increase (2nd to 8th hour) in plasma aldosterone to 2,6, and 9 times control values, respectively, in dogs receiving 40 mEq Na+/day. But, after the 1st day, aldosterone averaged only 1, 1.7, and 3 times control values for the next 2 weeks at the same rates of A II infusion. Dogs receiving 120 mEq Na+/day during A II infusion exhibited only a transient increase in plasma aldosterone during the 1st day. Sustained hypertension developed over a period of a week at all doses of A II at normal and high sodium intake, but did not occur at any dose of A II in sodium-depleted dogs. Increasing sodium intake from 40 to 120 mEq/day resulted in higher levels of hypertension, 125% compared to 140% of ocntrol values for dogs infused with A II, 5.0 ng/kg per min. We conclude that primary angiotensin-induced hypertension need not be associated with increased levels of plasma aldosterone, which appears to remain elevated only with amounts of A II greater than those required to sustain a significant degree of hypertension.

This article has been cited by other articles:

				J. P Collister and D. B Nahey Changing dietary sodium alters the chronic cardiovascular effects of losartan in rats Journal of Renin-Angiotensin-Aldosterone System, March 1, 2008; 9(1): 10 - 16. [Abstract] [PDF]

				S. G. Hood, T. Cochrane, M. J. McKinley, and C. N. May Investigation of the mechanisms by which chronic infusion of an acutely subpressor dose of angiotensin II induces hypertension Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2007; 292(5): R1893 - R1899. [Abstract] [Full Text] [PDF]

				L. P. LaGrange, G. M. Toney, and V. S. Bishop Effect of Intravenous Angiotensin II Infusion on Responses to Hypothalamic PVN Injection of Bicuculline Hypertension, December 1, 2003; 42(6): 1124 - 1129. [Abstract] [Full Text] [PDF]

				J. W. Osborn, P. Ariza-Nieto, J. P. Collister, S. Soucheray, B. Zimmerman, and S. Katz Responsiveness vs. basal activity of plasma ANG II as a determinant of arterial pressure salt sensitivity Am J Physiol Heart Circ Physiol, November 1, 2003; 285(5): H2142 - H2149. [Abstract] [Full Text] [PDF]

				B. C. Cholewa and D. L. Mattson Role of the renin-angiotensin system during alterations of sodium intake in conscious mice Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2001; 281(3): R987 - R993. [Abstract] [Full Text] [PDF]

				J.-M. LALOUEL, A. ROHRWASSER, D. TERREROS, T. MORGAN, and K. WARD Angiotensinogen in Essential Hypertension: From Genetics to Nephrology J. Am. Soc. Nephrol., March 1, 2001; 12(3): 606 - 615. [Abstract] [Full Text]

				S. N. Iyer, D. B. Averill, M. C. Chappell, K. Yamada, A. J. Allred, and C. M. Ferrario Contribution of Angiotensin-(1-7) to Blood Pressure Regulation in Salt-Depleted Hypertensive Rats Hypertension, September 1, 2000; 36(3): 417 - 422. [Abstract] [Full Text] [PDF]

				M. F. Callahan, P. Li, C. M. Ferrario, D. Ganten, and M. Morris Salt-Sensitive Hypertension in (mREN-2)27 Transgenic Rats Hypertension, March 1, 1996; 27(3): 573 - 577. [Abstract] [Full Text]