Abstract

Nicotine in concentrations ranging from 5 times 10- minus 6 to 10- minus 4 M caused a transient relaxation in strips of isolated canine basilar, middle cerebral and posterior cerebral arteries contracted with prostaglandin F2a (PGF). Transmural neural stimulation did not produce changes in the tension of these arteries. Tyramine contracted the arterial strips. Relaxation induced by nicotine was markedly attenuated by hexamethonium (10- minus 5 M), cocaine (10- minus 5M), bretylium (2 times 10- minus 5 M), sotalol (5 times 10- minus 5 M), propranolol (10- minus 6 M) and removal of Ca-++ from the bathing media. Relaxation was not significantly influenced by atropine, physostigmine, ouabain, tetrodotoxin, aminophylline and sotalol (10- minus 5 M). In cerebral arterial strips, the addition of K-+ also elicited a transient relaxation which was abolished by treatment with ouabain but not with other blocking agents. In mesenteric arterial strips, nicotine caused a transient contraction as did transmural stimulation. The nicotine-induced contraction was markedly attenuated or completely abolished by hexamethonium, cocaine, bretylium and phentolamine and also high concentration of sotalol (5 times 10- minus 5 M), and propranolol. Tetrodotoxin did not affect the contractile response to nicotine but did abolish the response to transmural stimulation. It is strongly suggested that relaxation induced by nicotine in cerebral arterial strips is the result of a specific action on nicotinic receptors as is the contraction observed in mesenteric arteries. It appears that beta adrenergic and cholinergic mechanisms do not play major roles in the genesis of nicotine-induced relaxation nor does it appear that an electrogenic Na-+ pump mechanism is involved.