dinoprost and sophoramine

In helical strips of dog mesenteric, coronary and cerebral arteries and mesenteric veins contracted with prostaglandin F2 alpha, sophoramine (10(-4) and 10(-3) M) produced a concentration-related relaxation, which was not influenced by treatment with indomethacin, atropine, aminophylline, propranolol, metoprolol, cimetidine, ouabain and methylene blue, and also not by removal of endothelium. Relaxations induced by sophoramine did not differ in strips of proximal and distal coronary arteries. Contractile responses to transmural stimulation in mesenteric arteries and veins were potentiated by treatment with sophoramine (10(-4) M). Treatment with cocaine, indomethacin, propranolol and saralasin did not alter the potentiating effect of sophoramine, whereas yohimbine, an alpha 2 adrenoceptor antagonist, attenuated it. Sophoramine did not significantly affect the contractile response to norepinephrine in mesenteric arteries and veins and the response to phenylephrine and clonidine in mesenteric veins. Sophoramine appears to non-specifically dilate dog arteries and veins and to facilitate the release of transmitter norepinephrine from adrenergic nerves via a mechanism of action on the prejunctional site sensitive to yohimbine.

Topics: Adrenergic Fibers; Alkaloids; Animals; Cerebral Arteries; Clonidine; Coronary Vessels; Dinoprost; Dogs; Dose-Response Relationship, Drug; Female; Male; Mesenteric Arteries; Mesenteric Veins; Muscle Relaxation; Muscle, Smooth, Vascular; Norepinephrine; Phenylephrine; Vasodilator Agents; Yohimbine