Effect of (Sar1, Ala8)-angiotensin II and hypophysectomy on the intestinal resistance vessels and blood pressure following furosemide-induced volume depletion.
Intravenous administration of furosemide (2 mg/kg) caused intestinal vasoconstriction in various groups of pentobarbital-anesthetized cats. (Sar1, Ala 8)-angiotensin II, a specific competitive antagonist of angiotensin II, was infused 60 min after administration of furosemide, a time when the intestinal vasoconstrictor response to the diuretic was maximal or near maximal. In hypophysectomized animals, infusion of the antagonist abolished the intestinal vasoconstriction and caused a significant fall in arterial pressure even when the intestinal nerves and adrenal glands remained intact. In contrast, the antagonist had little effect when the pituitary gland remained intact. The results suggest that endogenous angiotensin and vasopressin are overlapping mechanisms which constrict the intestinal resistance vessels and support arterial pressure following furosemide-induced volume depletion. In the absence of one control system, the other compensates to maintain the responses.
D000311:Adrenal Glands / Q000502:physiology; D000804:Angiotensin II / Q000031:analogs & derivatives*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001810:Blood Volume / Q000187:drug effects; D002415:Cats; D003714:Denervation; D005665:Furosemide / Q000494:pharmacology*; D007422:Intestines / Q000098:blood supply* / Q000294:innervation; D010902:Pituitary Gland / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects; D012504:Saralasin / Q000494:pharmacology*; D013997:Time Factors
D000804:Angiotensin II; D005665:Furosemide; D012504:Saralasin