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箭毒碱对大鼠阻力动脉血管舒张作用的相关机制。

Mechanisms involved in the vasodilator effect of curine in rat resistance arteries.

作者信息

Dias Celidarque S, Barbosa-Filho José M, Lemos Virgínia S, Côrtes Steyner F

出版信息

Planta Med. 2002 Nov;68(11):1049-51. doi: 10.1055/s-2002-35662.

Abstract

The vasodilator effect of curine was investigated in the rat small mesenteric arteries. In either endothelium-intact or endothelium-denuded mesenteric arteries, curine induced a concentration-dependent relaxation in rings pre-contracted with noradrenline (10 microM; IC 50 = 4.8 +/- 1.3 microM and 4.8 +/- 1.5 microM, respectively) and KCl (80 mM; IC 50 = 6.0 +/- 1.3 microM and 13.0 +/- 5.6 microM, respectively). Curine also inhibited (IC 50 = 4.6 +/- 0.9 microM) the concentration-response curves induced by noradrenaline. Contractions dependent on calcium-influx elicited by KCl (80 mM) and noradrenaline (10 microM) were inhibited by curine (10 microM). Finally, contractions induced by noradrenaline (10 microM), in calcium-free medium, were strongly inhibited by curine (10 microM). The above results suggest that the inhibition of influx of calcium ions through voltage-operated calcium channels and non-selective channels, and mobilization of intracellular calcium stores sensitive to noradrenaline are involved in the vasodilator effect of curine.

摘要

在大鼠小肠系膜动脉中研究了箭毒碱的血管舒张作用。在完整内皮或去内皮的系膜动脉中,箭毒碱均可使预先用去甲肾上腺素(10微摩尔;IC50分别为4.8±1.3微摩尔和4.8±1.5微摩尔)和氯化钾(80毫摩尔;IC50分别为6.0±1.3微摩尔和13.0±5.6微摩尔)预收缩的血管环产生浓度依赖性舒张。箭毒碱还抑制(IC50=4.6±0.9微摩尔)去甲肾上腺素诱导的浓度-反应曲线。箭毒碱(10微摩尔)可抑制由氯化钾(80毫摩尔)和去甲肾上腺素(10微摩尔)引起的依赖钙内流的收缩。最后,在无钙培养基中,箭毒碱(10微摩尔)可强烈抑制由去甲肾上腺素(10微摩尔)诱导的收缩。上述结果表明,箭毒碱的血管舒张作用涉及通过电压门控钙通道和非选择性通道抑制钙离子内流,以及动员对去甲肾上腺素敏感的细胞内钙储存。

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