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Mesaconitine-induced Relaxation in Rat Aorta: Involvement of Ca2+ Influx and Nitric-Oxide Synthase in the Endothelium

Mesaconitine-induced Relaxation in Rat Aorta: Involvement of Ca2+ Influx and Nitric-Oxide Synthase in the Endothelium

Mana Mitamura, Syunji Horie, Masaru Sakaguchi, Akiyoshi Someya, Shizuko Tsuchiya, Johan Van de Voorde, Toshihiko Murayama, Kazuo Watanabe

Eur J Pharmacol. 2002 Feb 2;436(3):217-25.

PMID: 11858801

Abstract:

Aconiti tuber, roots of aconite (Aconitum japonicum), is an oriental herbal medicine used for centuries in Japan and China to improve the health of persons with a weak constitution and poor metabolism. We investigated the effects of mesaconitine, one of the aconite alkaloids in Aconiti tuber, on the contraction and free intracellular Ca2+ concentration ([Ca2+]i) level in isolated rat thoracic aorta. Mesaconitine at 30 microM inhibited 3 microM phenylephrine-induced contraction in the endothelium-intact, but not endothelium-denuded, aortic rings. The effect of mesaconitine was dependent on external Ca2+ concentrations. The relaxation induced by mesaconitine was abolished by N(omega)-nitro-L-arginine methyl ester (0.1 mM, an inhibitor of nitric-oxide synthase), as well as the relaxation induced by acetylcholine. Acetylcholine induced relaxation in two phases in our conditions; the initial phase was transient and external Ca2+ -independent, and the second phase was sustained and external Ca2+ -dependent. Treatment with 100 nM thapsigargin, which depleted intracellular Ca2+ stores, inhibited acetylcholine-induced, but not mesaconitine-induced, relaxation. Mesaconitine increased the [Ca2+]i level in endothelial cells by influx of Ca2+ from extracellular spaces. These findings suggest that mesaconitine-induced Ca2+ influx and activation of nitric-oxide synthase in endothelial cells and, thus, induced vasorelaxation in rat aorta.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP2752649	Mesaconitine		2752-64-9	Price

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