阿托品对大鼠肠系膜动脉的舒张作用及机制

Vasodilation effect of atropine on rat mesenteric artery

目的 研究阿托品的扩血管作用及机制。方法 以大鼠肠系膜动脉为标本,考察阿托品对去甲肾上腺素(NE)预收缩血管的舒张作用以及血管内皮细胞、血管平滑肌在该效应中的作用。结果 阿托品能显著舒张NE预收缩的完整内皮血管,去内皮后该作用明显降低。L Nω硝基精氨酸甲酯、吲哚美辛、普萘洛尔及格列本脲对阿托品的舒张作用无明显影响。阿托品对KCl的量效曲线及咖啡因缩血管作用均无明显影响,但能浓度依赖性地抑制NE诱导的内钙释放以及经受体操纵性钙通道的外钙内流。结论 阿托品有明显的扩血管作用,其通过抑制受体介导的外钙内流和内钙释放而舒张血管。

Aim To study the vasodilation effect of atropine and its mechanism. Methods Isometric tension was recorded in isolated rat super mesenteric arteries precontracted by noradrenaline (NE) to study the vasodilation effect of atropine, and to investigate the role of endothelial cell and vascular smooth muscle cell on vasodilation. Results Atropine was shown to significantly dilate the endothelium-intact and endothelium-denuded arteries precontracted by NE. N^(ω)-Nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhibitor), indomethacin (cyclooxygenase inhibitor), propranolol (general β adrenoceptor antagonist ) and glibenclamide (ATP sensitive potassium channel inhibitor) showed no effect on vasodilation of atropine. Atropine did not affect the concentration-contraction curve of K^(+). However, atropine suppressed the contraction induced by NE and CaCl (2), but not that by caffeine in the Ca^(2+)-free Krebs solution. Conclusion Atropine showed significant vasodilation effect which may derive, in part, from endothelium. Besides, atropine could inhibit the receptor-mediated Ca^(2+)-influx and Ca^(2+)-release, which was inferred to the mechanism of atropine on vasodilation.