Influence of Experimental Subarachnoid Hemorrhage on Nicotine-induced Contraction of the Rat Basilar Artery in Relation to Nicotinic Acetylcholine Receptors, Calcium, and Potassium Channels

BackgroundCigarette smoking is associated with symptomatic vasospasm after subarachnoid hemorrhage (SAH).MethodsRat basilar arteries of a normal group and SAH groups (1 hour, 2 days, and 1 week) were removed from the brain and cut into spiral preparations.ResultsA central nervous system (CNS) nicotinic acetylcholine receptor (nAChR) and autonomic ganglionic nAChR antagonist (mecamylamine) and skeletal muscle nAChR antagonist (gallamine) concentration-dependently attenuated the nicotine-induced contraction. An autonomic ganglionic nAChR antagonist (hexamethonium) did not affect nicotine-induced contractions in normal rats or rats with SAH. The various nAChR antagonists showed no significant differences in their effects between normal and SAH (1 hour, 2 days, and 1 week) rats. An L-type Ca2+ channel antagonist (nifedipine) attenuated the nicotine-induced contraction in a concentration dependent manner. Inhibition by nifedipine was significantly enhanced in the 1-hour and 2-day SAH groups compared with normal and 1-week SAH groups. Levcromakalim showed a greater attenuation of nicotine-induced contraction in SAH (1 hour, 2 days, and 1 week) than in normal rats.ConclusionsNicotine-induced contraction of the rat basilar artery involved the CNS nAChR subfamily, skeletal muscle nAChR subfamily, and L-type Ca2+ channel pathways. SAH did not affect any of the subfamilies of nAChR, but the Ca2+ channel was reduced and the adenosine triphosphate–sensitive K+ channel was enhanced by SAH.