DILATATION OF MESENTERIC VASCULAR BED OF DOG PRODUCED BY A PEPTIDE, UROTENSIN I

Abstract

Urotensin I, a peptide derived from the urophysis of bony fish [Catostomus commersoni], produced hypotension when administered i.v. in small doses to pentobarbital-anesthetized dogs. The mechanism of this hypotensive response was mainly, if not exclusively, due to dilatation of the cephalic and caudal mesenteric arteries. Neither the hypotensive response nor the mesenteric vasodilator response was prevented by adrenergic, histaminergic or muscarinic receptor blockade [acetylcholine chloride, histamine dihydrochloride, I-norepinephrine bitartrate, dl-isoproterenol hydrochloride, dl-propranolol, diphenhydramine hydrochloride, burimamide hydrochloride, atropine sulfate and phenoxybenzamine hydrochloride]. In the doses employed, urotensin I inconstantly caused minimal increases in heart rate and left ventricular dp/dt [change in pressure with time]. These changes could be prevented by prior administration of propranolol, indicating that they were probably reflex in origin. The unique mechanism of action of the peptide may make it a valuable tool in studies of the mesenteric circulation, particularly in experimental shock; moreover, the peptide may prove useful in situations in which afterload reduction in the absence of cardiac stimulation is desired.