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. 1992 Jan;99(1):19-26.
doi: 10.1254/fpj.99.19.

[Mechanisms of histamine-induced relaxation in isolated dog mesenteric arteries and veins]

[Article in Japanese]
Affiliations

[Mechanisms of histamine-induced relaxation in isolated dog mesenteric arteries and veins]

[Article in Japanese]
M Yamazaki et al. Nihon Yakurigaku Zasshi. 1992 Jan.

Abstract

Mechanisms of histamine-induced relaxation in dog mesenteric artery and vein strips were compared. Histamine elicited a concentration-related relaxation in the arterial strips contracted with prostaglandin (PG) F2 alpha; the relaxations induced at 5 x 10(-7) M or higher were composed of phasic and tonic patterns. The phasic component of relaxation was inhibited by chlorpheniramine, but not by cimetidine. Combined treatment with the H1 and H2 antagonists abolished the amine-induced relaxation. The tonic component was inhibited by cimetidine. The phasic relaxation was attenuated by removal of the endothelium. Treatment with indomethacin inhibited the phasic component in the strips with endothelium, but did not influence the relaxation after endothelium denudation. Combined treatment with indomethacin and cimetidine, but not chlorpheniramine, abolished the response. On the other hand, histamine produced a concentration-related, tonic relaxation in the mesenteric vein strips. The relaxation was not influenced by indomethacin, endothelium-denudation, and chlorpheniramine, but was abolished by cimetidine. It may be concluded that the phasic relaxation of dog mesenteric arterial strips is mediated mainly by H1 receptors in the endothelium, resulting in the synthesis and release of PGI2. The tonic relaxation appears to be elicited by activation of H2 receptors in smooth muscle. Mesenteric vein relaxations induced by histamine are likely to be mediated solely by H2 receptors in smooth muscle.

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