AJP - Renal Physiology, Vol 252, Issue 6 992-1002, Copyright © 1987 by American Physiological Society

ARTICLES

Atriopeptin III alters renal medullary hemodynamics and the pressure-diuresis response in rats

K. Takezawa, A. W. Cowley Jr, M. Skelton and R. J. Roman

The effects of atriopeptin III on the renal response to changes in renal perfusion pressure (RPP) were examined in uninephrectomized and adrenalectomized rats. Neural influences on the kidney were eliminated by renal denervation. Plasma levels of antidiuretic hormone (ADH), angiotensin II, aldosterone, corticosterone, and norepinephrine were controlled by intravenous infusion. Infusion of atriopeptin III at a dose of 30 or 100 ng X kg-1 X min-1 increased plasma levels of atrial natriuretic peptide from 101 +/- 8 pg/ml to 424 +/- 16 and 2,553 +/- 308 pg/ml, respectively. In control rats, increasing RPP in two steps from 100 to 125 to 150 mmHg produced sixfold increases in sodium and water excretion. The slopes of the relationships between fractional sodium and water excretion and RPP were enhanced by approximately 10, 20, and 40% in the rats infused with the 30, 100, and 500 ng X kg-1 X min-1 dose of atriopeptin III. Renal blood flow and glomerular filtration rate were not significantly different in vehicle- and atriopeptin III-infused rats at any RPP studied. Papillary blood flow measured with a laser-Doppler flowmeter increased 15% within the first 5 min of infusion of atriopeptin III at a dose of 100 ng X kg-1 X min-1. Cortical blood flow was not significantly altered. The rise in papillary blood flow during atriopeptin III infusion, however, may be a consequence and not the cause of the natriuresis and diuresis, since urine flow increased before significant changes in papillary blood flow were detected. These studies suggest that atrial natriuretic factor could influence the long-term control of arterial pressure by altering renal medullary hemodynamics and promoting the elimination of sodium and water. The plasma levels of atrial natriuretic peptide needed to alter the pressure-natriuresis relationship, however, may exceed levels that can be attained in vivo with endogenous release.

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