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目的:研究川芎素(SF)对犬冠脉的舒张作用及机制。方法:以犬冠脉为标本,用去甲肾上腺素(NE)和氯化钾(KCl)刺激标本收缩,研究SF对NE和KCl致动脉收缩量效曲线的影响并测定pD2ˊ以考察其对电压依赖性和受体操纵性钙通道的影响;制作SF对NE和KCl致动脉收缩的抑制作用量效曲线以测定其IC50,进一步判断SF阻滞钙通道的作用强度;观察SF对NE致动脉收缩两种组分的影响,考察其对受体操纵性外钙内流和内钙释放的影响。结果:SF使NE和KCl收缩冠脉的量效曲线非平行右移,其非竞争性阻断NE和KCl的pD2ˊ分别为3.65±0.22和3.58±0.10。SF剂量依赖性地抑制NE和KCl引起的冠脉收缩,IC50分别为1.04±0.68×10-4和1.53±0.34×10-4M。SF剂量依赖性地抑制NE依内、外源性钙收缩。结论:SF可抑制NE和KCl引起的冠脉收缩,机制涉及抑制平滑肌细胞电压依赖性钙通道和受体操纵钙通道介导的外钙内流和内钙释放,但作用不强。
Objective: To study the relaxing effect and mechanism of sodium ferulate on canine coronary artery. Methods: The canine coronary artery was used as a sample. Norepinephrine (NE) and potassium chloride (KCl) were used to stimulate the contraction of the specimens. The effects of SF on NE volumetric contraction and contraction induced by NE and KCl were investigated. Dependent and receptor-manipulating calcium channels. The inhibitory effect of SF on NE and KCl-induced arterial constriction was measured to determine the IC50, and the effect of SF on calcium channel was further evaluated. The effects of two components on the extracellular Ca2 + influx and intracellular Ca2 + release were investigated. RESULTS: SF did not shift the dose-response curves of NE and KCl contracting coronary arteries to the right. The pD2’of noncompetitive blocking NE and KCl were 3.65 ± 0.22 and 3.58 ± 0.10, respectively. SF dose-dependently inhibited NE and KCl induced coronary contractions with IC50 of 1.04 ± 0.68 × 10-4 and 1.53 ± 0.34 × 10-4 M, respectively. SF dose-dependently inhibited NE-mediated extrinsic calcium contraction. CONCLUSIONS: SF inhibits coronary artery contractility induced by NE and KCl, and its mechanism is involved in the inhibition of voltage-dependent Ca2 + channel and receptor Ca2 + channel-mediated Ca2 + influx and Ca2 + release in smooth muscle cells.