Relaxant Effects of Matrine on Aortic Smooth Muscles of Guinea Pigs

Objective To determine whether matrine, a kind of traditional Chinese medicinal alkaloid, can relax the aortic smooth muscles isolated from guinea pigs and to investigate the mechanism of its relaxant effects. Methods Phenylephrine or potassium chloride concentration-dependent relaxation response of...

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Veröffentlicht in:Biomedical and environmental sciences 2009-08, Vol.22 (4), p.327-332, Article 327
Hauptverfasser: ZHENG, JIE, ZHENG, PING, ZHOU, XU, YAN, LIN, ZHOU, RU, FU, XUE-YAN, DAI, GUI-DONG
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Sprache:eng
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Zusammenfassung:Objective To determine whether matrine, a kind of traditional Chinese medicinal alkaloid, can relax the aortic smooth muscles isolated from guinea pigs and to investigate the mechanism of its relaxant effects. Methods Phenylephrine or potassium chloride concentration-dependent relaxation response of aortic smooth muscles to matrine was studied in the precontracted guinea pigs. Results Matrine (1×10^-4 mol/L -3.3×10^-3 mol/L) relaxed the endothelium-denuded aortic rings pre-contracted sub-maximally with phenylephrine, in a concentration-dependent manner, and its pre-incubation (3.3× 10^- 3 mol/L) produced a significant rightward shift in the phenylephrine dose-response curve, but had no effects on the potassium chloride-induced contraction. The anti-contractile effect of matrine was not reduced by the highly selective ATP-dependent K^+ channel blocker glibenclamide (10.5 mol/L), either by the non-selective K^+channel blocker tetraethylammonium (10^-3 mol/L), or by the β-antagonist propranolol (10^-5 mol/L). In either "normal" or "Ca^2+-free" bathing medium, the phenylephrine-induced contraction was attenuated by matrine (3.3×10^-3 mol/L), indicating that the vasorelaxation was due to inhibition of intracellular and extracellular Ca^2+ mobilization. Conclusion Matrine inhibits phenylephrine-induced contractions by inhibiting activation of α-adrenoceptor and interfering with the release of intracellular Ca^2+ and the influx of extracellular Ca^2+.
ISSN:0895-3988
2214-0190
DOI:10.1016/S0895-3988(09)60063-5