Abstract
The mechanism of autoregulation of renal blood flow was investigated in anesthetized dogs, using either constant-flow or constant-pressure perfusion of the kidney. Prostaglandinlike material in the renal venous blood was assayed by the blood-bathed organ technique. Compensatory renal vasodilation, induced either by lowering the blood flow or the perfusion pressure, was accompanied by increased output of prostaglandinlike material into the renal venous blood. The prostaglandin synthetase inhibitor, indomethacin, abolished this output, and, at the same time, autoregulation of renal blood flow was abolished. A converting enzyme inhibitor, however, had no effect on renal autoregulation. The results support the hypothesis that autoregulation in the kidney is mediated by release of a vasodilator, prostaglandin, rather than by formation of a vasoconstrictor substance such as angiotensin II.
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