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Vol. 284, Issue 2, 790-797, February 1998
Department of Pharmacology, Southern Illinois University School of
Medicine, Springfield, IL, U.S.A. (W.Z., T.J-F.L.) and
Department of
Internal Medicine, University Hospital of Lund, Lund University, Lund,
Sweden (L.E)
The present experiment was designed to examine possible influence of
adrenergic nerves on nicotine-induced neurogenic vasodilation in
porcine basilar arteries denuded of endothelium. Nicotine and transmural nerve stimulation (TNS) induced relaxation of basilar arteries. Tetrodotoxin (TTX) abolished the relaxation elicited by TNS,
but only partially blocked that induced by nicotine. Relaxation induced
by both nicotine and TNS was abolished by
N-nitro-L-arginine. The N-nitro-L-arginine
inhibition of both TNS- and nicotine-induced relaxation was reversed by
L-arginine but not by D-arginine. Hexamethonium abolished the relaxation induced by nicotine, but did not affect that
elicited by TNS. Relaxation induced by nicotine was diminished by
guanethidine, which did not affect the relaxation induced by TNS,
suggesting that guanethidine blockade of nicotine-induced relaxation is
not due to its local anesthetic effect. Results from histochemical
studies indicated that catecholamine fluorescence and NADPH-diaphorase
fibers were not appreciably affected by guanethidine. Following
incubation with 6-hydroxydopamine for 1 hr, the catecholamine fluorescence fibers in the basilar arteries completely disappeared, although the NADPH-diaphorase fibers were not affected. In these adrenergically denervated arteries, nicotine-induced relaxation was
abolished, while the TNS-elicited relaxation was not affected. Furthermore, norepinephrine-induced relaxation in basilar arteries was
blocked by N-nitro-L-arginine, but was not affected by
N-nitro-D-arginine or hexamethonium. These results suggest
that in porcine cerebral arteries nicotine-induced nitric
oxide-mediated relaxation is dependent on an intact adrenergic
innervation. Nicotine appears to act on nicotinic receptors on the
presynaptic adrenergic nerve terminals to release norepinephrine or a
related substance, which then stimulates release of nitric oxide from
the neighboring nitric oxidergic nerves. The TNS-elicited nitric
oxide-mediated relaxation, however, is resulted from direct
depolarization of nitric oxidergic nerves.
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