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AJP - Renal Physiology, Vol 258, Issue 5 1232-F1236, Copyright © 1990 by American Physiological Society
ARTICLES |
D. L. Stacy, J. W. Scott and J. P. Granger
Department of Physiology, Eastern Virginia Medical School, Norfolk 23501.
It has been demonstrated that bolus injections of a vasoconstrictor derived from endothelial cells, endothelin 1 (ET-1), constricts isolated arteries and increases blood pressure in animals when infused intravenously. The purpose of this study was to examine the direct effects of intrarenal infusions of ET-1 on renal function at doses that do not alter systemic arterial pressure. The effects of ET-1 on renal hemodynamics and electrolyte excretion were examined during 40 min of intrarenal infusions of ET-1 at rates of 1.15 and 5 ng.kg-1.min-1. Infusion of ET-1 (1.15 ng.kg-1.min-1) resulted in a transient increase in renal blood flow (RBF) followed by a progressive vasoconstriction, which reduced RBF by 23%. ET-1 decreased glomerular filtration rate (GFR) and had no significant effect on filtration fraction. Intrarenal infusion of ET-1 (1.15 ng.kg-1.min-1) had no effect on fractional excretion of sodium (FENa) or potassium. Infusion of ET-1 at a higher dose (5 ng.kg-1.min-1) produced further reductions in RBF, GFR, and FENa. These data indicate that ET-1 is a potent renal vasoconstrictor that could play a role in controlling renal hemodynamics.
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