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目的:研究肌浆网钙泵抑制是否参与H_2O_2诱导的大鼠主动脉收缩反应。方法:离体主动脉环张力实验比较H_2O_2及钙泵特异性抑制剂环匹阿尼酸(CPA)缩血管效应及其信号机制的差异。结果:H_2O_2和CPA均收缩去内皮主动脉环,但H_2O_2触发快速短暂相位相收缩,而CPA诱导缓慢持续的张力相收缩。在无钙液中,仅CPA30μmol/L而非H_2O_230μmol/L预处理取消苯肾上腺素10μmol/L缩血管效应。Thap-sigargin 30μmol/L诱导最大收缩反应时,仅H_2O_2能使血管环进一步收缩。另外,P_2受体拮抗剂suramin、RB-2(各100μmol/L)以及多种酶抑制剂包括PLC、PKC、PLA_2、COX和蛋白质酪氨酸激酶均能抑制H_2O_2而非CPA诱导的缩血管效应,但2-APB50μmol/L对两者都有抑制作用。结论:肌浆网钙泵抑制不是H_2O_2收缩大鼠去内皮主动脉的机制。
AIM: To investigate whether inhibition of sarcoplasmic reticulum calcium pump is involved in H 2 O 2 -induced aortic contractions in rats. Methods: Tension experiments of isolated aortic rings were used to compare the vasoconstrictive effects of H 2 O 2 and CPP, a specific calcium pump inhibitor, and their signaling mechanisms. RESULTS: H 2 O 2 and CPA both contracted to the aortic rings, but H 2 O 2 triggered rapid and transient phase contractions while CPA induced slow and sustained contractions. In calcium-free solution, preconditioning with 30 μmol / L of CPA alone instead of H 2 O 2 30 μmol / L abolished the vasorelaxation effect of 10 μmol / L phenylephrine. When Thap-sigargin induced maximal contractile response at 30μmol / L, only H_2O_2 could further vasoconstriction. In addition, p2 receptor antagonists suramin, RB-2 (each 100μmol / L) and various enzyme inhibitors including PLC, PKC, PLA_2, COX and protein tyrosine kinases can inhibit H 2 O 2 rather than CPA induced vasoconstriction , But 2-APB50μmol / L had an inhibitory effect on both. Conclusions: The inhibition of sarcoplasmic reticulum calcium pump is not the mechanism of H 2 O 2 contraction in rats.