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

• Published in: Journal of stroke and cerebrovascular diseases 2013-05, Vol.22 (4), p.371-377
• Main Authors: Ji, Xu, PhD, Wang, Aimin, MS, Trandafir, Cristina C., PhD, Kurahashi, Kazuyoshi, PhD
• Format: Article
• Language: English
• Subjects: Adenosine triphosphate–sensitive K+ channel; Animals; Basilar Artery - drug effects; Basilar Artery - metabolism; Basilar Artery - physiopathology; Calcium Channel Blockers - pharmacology; Calcium Channels, L-Type - drug effects; Calcium Channels, L-Type - metabolism; Cardiovascular; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Ganglionic Blockers - pharmacology; KATP Channels - drug effects; KATP Channels - metabolism; L-type Ca2+ channel; Neurology; Nicotine - pharmacology; nicotine-induced contraction; nicotinic acetylcholine receptors; Nicotinic Agonists - pharmacology; Nicotinic Antagonists - pharmacology; Rats; Rats, Sprague-Dawley; Receptors, Nicotinic - drug effects; Receptors, Nicotinic - metabolism; subarachnoid hemorrhage; Subarachnoid Hemorrhage - metabolism; Subarachnoid Hemorrhage - physiopathology; Vasoconstriction - drug effects; Vasoconstrictor Agents - pharmacology
• ISSN: 1052-3057; 1532-8511
• DOI: 10.1016/j.jstrokecerebrovasdis.2011.09.020

Background Cigarette smoking is associated with symptomatic vasospasm after subarachnoid hemorrhage (SAH). Methods Rat 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. Results A 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. Conclusions Nicotine-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.