AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 6 1445-R1452, Copyright © 1990 by American Physiological Society
Atrial natriuretic peptide induces sustained natriuresis in conscious dogs
H. L. Mizelle, D. A. Hildebrandt, C. A. Gaillard, M. W. Brands, J. P. Montani, M. J. Smith Jr and J. E. Hall
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
Although acute infusions of atrial natriuretic peptide (ANP) often cause
natriuresis, these effects are not sustained, possibly because of
reductions in arterial pressure or other compensatory adaptations. The aim
of this study was to determine whether physiological increases in
intrarenal ANP levels cause sustained natriuresis if changes in arterial
pressure and other neurohumoral influences that might obscure the renal
responses are controlled. Changes in renal function were quantitated during
chronic unilateral renal arterial infusion of ANP at rates of 1, 2, and 4
ng.kg-1.min-1 in conscious dogs (n = 7) with the urinary bladder split to
allow continuous measurement of renal excretion in the ANP-infused and
contralateral, vehicle-infused kidneys. There was no change in mean
arterial pressure at any infusion rate. During 1 ng.kg-1.min-1 infusion of
ANP for 5 days, the renal excretory responses were small and variable.
However, during 2 and 4 ng.kg-1.min-1 ANP infusion for 7 days, sodium
excretion averaged 37.2 +/- 10.0 and 134.8 +/- 19.0% greater, respectively,
in the ANP-infused kidneys compared with the vehicle-infused kidneys but
there were no changes in glomerular filtration rate or effective renal
plasma flow. These results demonstrate that when compensatory changes in
arterial pressure and neurohumoral factors are controlled, ANP, at
physiological concentrations, causes marked increases in renal excretion.
This study supports the concept that ANP's effects to increase renal
excretory capability could play a role in long-term control of arterial
pressure and body fluid homeostasis.
