Mechanism of nicotine-induced relaxation in dog cutaneous arteries

Mechanism underlying relaxations induced by nicotine was analyzed in isolated dog cutaneous arterial strips without the endothelium. In the strips treated with prazosin and α,β-methylene ATP, nicotine produced relaxations, which were abolished by treatment with hexamethonium. Relaxations induced by...

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Bibliographic Details
Published in:Japanese Journal of Pharmacology 1996, Vol.71 (suppl.1), p.142-142
Main Authors: Uchiyama, Masami, Ayajiki, Kazuhide, Okamura, Tomio, Toda, Noboru
Format: Article
Language:eng ; jpn
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Summary:Mechanism underlying relaxations induced by nicotine was analyzed in isolated dog cutaneous arterial strips without the endothelium. In the strips treated with prazosin and α,β-methylene ATP, nicotine produced relaxations, which were abolished by treatment with hexamethonium. Relaxations induced by nicotine were partially inhibited by N^G -nitro-L-arginine (L-NA); the remaining relaxations were abolished by desensitization to calcitonin gene-related peptide (CGRP) or treatment with [8-37]CGRP or capsaicin. Desensitization to vasoactive intestinal polypeptide (VIP) or a VIP receptor antagonist did not influence the nicotine-induced relaxations. In the strips desensitized to CGRP, the nicotine-induced relaxations were abolished by L-NA. The inhibitory effect of L-NA was reversed by L-arginine. Perivascular nerves containing NADPH diaphorase and CGRP immunoreactivity were observed in the adventitia. It appears that the nicotine-induced relaxation is associated with stimulation of vasodilator nerves liberating NO and CGRP.
ISSN:0021-5198
DOI:10.1016/S0021-5198(19)36807-6