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*Compound via MeSH
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Hazardous Substances DB
*NICOTINE
*NICOTINE TARTRATE
*NITRIC OXIDE

Vol. 298, Issue 1, 122-128, July 2001

Presynaptic alpha 7-Nicotinic Acetylcholine Receptors Mediate Nicotine-Induced Nitric Oxidergic Neurogenic Vasodilation in Porcine Basilar Arteries

Min-Liang Si and Tony J. F. Lee

Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, Illinois

We previously reported that nicotine-induced nitric oxide (NO)-mediated neurogenic vasodilation in the porcine basilar artery was dependent on intact sympathetic innervation. We further demonstrated in this artery that nicotine acted on nicotinic acetylcholine receptors (nAChRs) on presynaptic sympathetic nerve terminals to release norepinephrine (NE), which then acted on beta 2-adrenoceptors located on the neighboring NOergic nerve terminals to release NO, resulting in vasodilation. The nature of the nAChRs has not been determined. The nAChR subtype mediating nicotine-induced dilation in isolated porcine basilar arterial rings denuded of endothelium was therefore examined pharmacologically and immunohistochemically. Results from using an in vitro tissue bath technique indicated that relaxation induced by nicotine (100 µM) was blocked by preferential alpha 7-nAChR antagonists (methyllycaconitine and alpha -bungarotoxin) and nonspecific nAChR antagonist (mecamylamine) in a concentration-dependent manner, but was not affected by dihydro-beta -erythroidine (a preferential alpha 4-nAChR antagonist). These nAChR antagonists did not affect relaxation elicited by transmural nerve stimulation (8 Hz) or that by sodium nitroprusside and NE. Results from double-labeling immunohistochemical studies in whole-mount porcine basilar and middle cerebral arteries and in cultured porcine superior cervical ganglia (SCG) indicated that alpha 7-nAChR- and tyrosine hydroxylase immunoreactivities were colocalized in same nerve fibers. These results suggest the presence of functional alpha 7-nAChRs on postganglionic sympathetic adrenergic nerve terminals of SCG origin, which mediate nicotine-induced neurogenic NOergic vasodilation. These findings are consistent with our hypothesis that nicotine acts on nAChRs on presynaptic sympathetic nerve terminals to release NE, which then acts on presynaptic beta 2-adrenoceptors located on the neighboring NOergic nerve terminals, resulting in release of NO and dilation of porcine basilar arteries.

0022-3565/01/2981-0122$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2001 by The American Society for Pharmacology and Experimental Therapeutics


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