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RISS 인기검색어
- 검색키워드
- 저자 : Cang-Bao Xu (검색결과 3 건)
- 무료
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- 유료
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Dimethylsulfoxide-soluble Smoking Particles and Nicotine Affect Vascular Contractibility
Jin-Yan Zhang,Lei Cao,Cang-Bao Xu,Yong-Xiao Cao,Xiao-Hui Zheng 대한약학회 2009 Archives of Pharmacal Research Vol.32 No.10
The aim is to study the effect of dimethylsulfoxide-soluble smoking particles (DSP) and nicotine on the contractility of rat mesenteric artery. The superior mesenteric artery segments were cultured with DSP or nicotine for 24 h. The vascular contractibility was recorded with myograph system. DSP 0.4 mL/L and nicotine 0.48 and 0.96 mg/L shifted the concentrationcontractile curves induced by sarafotoxin 6c, a selective agonist for ETB receptor toward the left with increased Emax. DSP 0.4 mL/L and nicotine 0.96 mg/L shifted ETA receptor-mediated the concentration-contractile curves toward the left with increased Emax. However, nicotine 0.06 mg/L which is the equivalent concentration of nicotine in DSP 0.4 mL/L did not affect the curves and the Emax mediated with ETA receptor and ETB receptor. DSP 0.2 and 0.4 mL/L shifted the concentration-contractile curves induced by noradrenaline toward the right with decreased Emax. Neither did nicotine 0.06 and 0.96 mg/L. Both DSP and nicotine shifted the concentration-contractile curves induced by 5-hydroxytryptamine (5-HT) toward the right parallely. DSP changed the phenotypes towards an increased efficacy of ETA receptor and ETB receptor, and a reduced efficacy of 5-HT receptor and α-adrenocceptor. The effects of DSP on ETB receptor, ETA receptor and α-adrenocceptor were independent of nicotine. The effect on 5-HT receptor was responsible to nicotine.
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Yong-Xiao Cao,Jian-Pu Zheng,Jian-Yu He,Jie Li,Cang-Bao Xu,Lars Edvinsson 대한약학회 2005 Archives of Pharmacal Research Vol.28 No.6
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 µM, 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 α1-adrenoreceptor. The β- 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 CaCl2 in Ca2+-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular Ca2+ influx through the receptoroperated calcium channels and intracellular Ca2+ release from the Ca2+ store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular Ca2+ 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 Ca2+-influx and Ca2+- release, and partly from the endothelium mediated by EDHF.
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Cao Yong-Xiao,Zheng Jian-Pu,He Jian-Yu,Li Jie,Xu Cang-Bao,Edvinsson Lars The Pharmaceutical Society of Korea 2005 Archives of Pharmacal Research Vol.28 No.6
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.
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