AJP - Renal Physiology, Vol 249, Issue 2 299-F307, Copyright © 1985 by American Physiological Society

ARTICLES

Mechanisms of angiotensin II natriuresis and antinatriuresis

M. E. Olsen, J. E. Hall, J. P. Montani, A. C. Guyton, H. G. Langford and J. E. Cornell

The aim of this study was to determine the role of changes in renal arterial pressure (RAP), renal hemodynamics, and tubular reabsorption in mediating the natriuretic and antinatriuretic actions of angiotensin II (ANG II). In seven anesthetized dogs, endogenous ANG II formation was blocked with captopril, and ANG II was infused intravenously at rates of 5-1,215 ng X kg-1 X min-1 while RAP was either servo-controlled at the preinfusion level or permitted to increase. When RAP was servo-controlled, ANG II infusion at all rates from 5-1,215 ng X kg-1 X min-1 decreased urinary sodium excretion (UNaV) and fractional sodium excretion (FENa) while increasing fractional reabsorption of lithium (FRLi) (an index of proximal tubular fractional sodium reabsorption) and causing no change in calculated distal tubule fractional sodium reabsorption (FRDNa). When RAP was permitted to increase, ANG II infusion rates up to 45 ng X kg-1. min-1 also decreased UNaV and FENa while increasing FRLi and causing no change in FRDNa. However, at 135 ng X kg-1 X min-1 and above, UNaV and FENa increased while FRLi and FRDNa decreased when RAP was allowed to rise, even though renal blood flow and filtration fraction were not substantially different from the values observed when RAP was servo-controlled. Filtered sodium load was slightly higher when RAP was permitted to increase during ANG II infusion compared with when RAP was servo-controlled, although the differences were not statistically significant. Thus, even very large doses of ANG II cause antinatriuresis when RAP is prevented from increasing.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				V. Pech, Y. H. Kim, A. M. Weinstein, L. A. Everett, T. D. Pham, and S. M. Wall Angiotensin II increases chloride absorption in the cortical collecting duct in mice through a pendrin-dependent mechanism Am J Physiol Renal Physiol, March 1, 2007; 292(3): F914 - F920. [Abstract] [Full Text] [PDF]

				J. D. Klein, B. P. Murrell, S. Tucker, Y.-H. Kim, and J. M. Sands Urea transporter UT-A1 and aquaporin-2 proteins decrease in response to angiotensin II or norepinephrine-induced acute hypertension Am J Physiol Renal Physiol, November 1, 2006; 291(5): F952 - F959. [Abstract] [Full Text] [PDF]

				S. H. Padia, N. L. Howell, H. M. Siragy, and R. M. Carey Renal Angiotensin Type 2 Receptors Mediate Natriuresis Via Angiotensin III in the Angiotensin II Type 1 Receptor-Blocked Rat Hypertension, March 1, 2006; 47(3): 537 - 544. [Abstract] [Full Text] [PDF]

				M. Schou, A. Gabrielsen, N. E. Bruun, P. Skott, B. Pump, H. Dige-Petersen, E. Frandsen, P. Bie, J. Warberg, N. J. Christensen, et al. Angiotensin II attenuates the natriuresis of water immersion in humans Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2002; 283(1): R187 - R196. [Abstract] [Full Text] [PDF]

				M. K. Heinz and D. A. Gray Role of plasma ANG II in the excretion of acute sodium load in a bird with salt glands (Anas platyrhynchos) Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2001; 281(1): R346 - R351. [Abstract] [Full Text] [PDF]

				T. Traynor, T. Yang, Y. G. Huang, J. H. Krege, J. P. Briggs, O. Smithies, and J. Schnermann Tubuloglomerular feedback in ACE-deficient mice Am J Physiol Renal Physiol, May 1, 1999; 276(5): F751 - F757. [Abstract] [Full Text] [PDF]