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作 者:彭晓云[1] 温绍君[2] 陶燕铎[1] 于庆利[2] 王佐广[2] 梅丽娟[1] 赵利敏[2] 王绿娅[2]
机构地区:[1]中国科学院西北高原生物研究所,西宁810001 [2]北京心肺疾病研究所北京安贞医院高血压研究室,北京100029
出 处:《中药药理与临床》2003年第2期43-45,共3页Pharmacology and Clinics of Chinese Materia Medica
摘 要:目的 :通过观察藏药 1号水提液对大鼠离体胸动脉条收缩作用的影响研究其降压机制。方法 :观察藏药 1号水提液( 6mg/mL)和维拉帕米 (Ver 0 .0 13mg/mL)对高K+ 液引起的主动脉条收缩的时效影响 ,对KCl,NE及CaCl2 引起的大鼠主动脉条收缩的量效曲线的影响 ,以及对NE引起的依赖于细胞内钙及细胞外钙的收缩的影响。结果 :藏药 1号水提液抑制高K+ 液引起的主动脉收缩 ;且可使KCl、NE及CaCl2 引起的大鼠主动脉条收缩的量效曲线非平行右移 ,最大效应降低 ,呈非竞争性拮抗作用 ;与维拉帕米相似 ,对NE引起的依赖于细胞内钙及细胞外钙的收缩均有抑制作用。结论 :提示藏药 1号的降压机制与钙离子通道拮抗剂一致。Objective: To study the influence of aqueous extract from ZangYao-I(AEZY-I) on inhibition to the contractions induced by KCl, NE, CaCl_2 in isolated rat thoracic aortic rings, and uncover the mechanism of antihypertensive effect of ZanyYao-I. Methods: Recording the dose-response curves induced by KCl, NE, CaCl_2, and the next dose-response curves again after AEZY-I being added, respectively. Results: AEZY-I inhibited the contractions evoked by KCl, NE, CaCl_2 in isolated rat thoracic aortic rings. Significantly, AEZY-I could depress the maximal response and cause rightward displacement of the dose-response curves, and resulted of a non-competitive antagonism mechanism. In Ca 2+ free solution, AEZY-I inhibited contraction in aortic rings, which is dependent on Ca 2+ relased from not only intracellular store but also extracellular Ca 2+ . Therefore, AEZY-I inhibited both the potential dependent channel and the receptor operated channel. Conclusion: AEZY-I could relax the contraction of isolated rat thoracic aortic rings, and so the mechanism of antihypertensive of ZangYao-I is related to its antagonistic effect on calcium ion.
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