Intestinal Vasoconstriction following Diuretic-Induced Volume Depletion: Role of Angiotensin and Vasopressin

Abstract

Intravenous administration of furosemide, ethacrynic acid, or chlorothiazide induced intestinal vasoconstriction in pentobarbital-anesthetized cats. The vasoconstrictor response following furosemide was prevented by nephrectomy or by replacement of urinary losses, indicating the response was dependent upon the volume-depletion produced by the drug. The intestinal vasoconstriction following furosemide was not reduced in animals subjected to acute intestinal denervation, adrenalectomy, and hypophysectomy. Similarly the response was not reduced in animals subjected to intestinal denervation and adrenalectomy, and administered SQ20881, an inhibitor of angiotensin-converting enzyme. However, administration of SQ20881 to hypophysectomized animals completely abolished the vasoconstriction even when the intestinal innervation and adrenal glands remained intact. The results suggest that the renin–angiotensin system and the vasopressin system play major roles in the mechanism of the intestinal vasoconstriction following diuretic-induced volume depletion and that the sympathoadrenal system plays little role in this response.