Induces Vasodilatation of Rat Mesenteric Artery in vitro Mainly by Inhibiting Receptor-Mediated $Ca^{2+}$ -Influx and $Ca^{2+}$ -Release

Cao Yong-Xiao; Zheng Jian-Pu; He Jian-Yu; Li Jie; Xu Cang-Bao; Edvinsson Lars

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자료유형: 학술저널

저자정보: Cao Yong-Xiao (Department of Pharmacology, Medical School of Xi'an Jiaotong University, and Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University, Ministry of Education) Zheng Jian-Pu (Department of Pharmacology, Medical School of Xi'an Jiaotong University, and Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University, Ministry of Education) He Jian-Yu (Department of Pharmacology, Medical School of Xi'an Jiaotong University, and Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University, Ministry of Education) Li Jie (Department of Pharmacology, Medical School of Xi'an Jiaotong University, and Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University, Ministry of Education) Xu Cang-Bao (Department of Pharmacology, Medical School of Xi'an Jiaotong University, and Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong Univer) Edvinsson Lars

저널정보: 대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제28권 제6호

발행연도: 2005.1

수록면: 709 - 715 (7page)

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The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1$\mu$M, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the ${\alpha}_1$-adrenoreceptor. The $\beta$-adrenoreceptor and ATP sensitive potassium channel, a voltage dependent calcium channel, were not involved in the vasodilatation. However, atropine inhibited the contraction derived from NA and $CaCl_2$ in $Ca^{2+}$-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular $Ca^{2+}$ influx through the receptor-operated calcium channels and intracellular $Ca^{2+}$ release from the $Ca^{2+}$ store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular $Ca^{2+}$ release as a result of atropine most likely occurs via the IP3 pathway rather than the ryanodine receptors. Our results suggest that atropine-induced vasodilatation is mainly from artery smooth muscle cells due to inhibition of the receptor-mediated $Ca^{2+}$-influx and $Ca^{2+}$-release, and partly from the endothelium mediated by EDHF.

#Atropine #Vasodilatation #Rat mesenteric artery #null #EDHF

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