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目的:研究胞内钙动员在硝普钠(SNP)增加豚鼠胃窦环行平滑肌细胞钙敏感性钾电流[I_((K(Ca))]中的作用。方法:采用传统全细胞膜片箝技术,并用胶原酶急性分离单细胞。用硝普钠作为一氧化氮供体。结果:SNP100 μmol/L明显增加钙敏感性钾电流,同时也可以显著地增加瞬间外向性钾电流(STOC)。SNP引发I_(K(Ca))增加效应不能被胞外无钙液(含依他酸10 μmol/L)和L-型钙通道阻断剂尼卡地平5 μmol/LL所阻断。SNP100 μmol/L可以明显地抑制钙电流。SNP引发STOC增加效应可以明显地被三磷酸肌醇受体特异性阻断剂肝素3 g/L所阻断,却不能被兰尼碱10 μmol/L所阻断。亚甲基蓝1 μmol/L,特异性胞内鸟苷酸环化酶抑制剂,也可以显著地抑制上述效应。结论:SNP引发钙敏感性钾电流的增加可能是胞内第二信使cGMP通过激活胞内三磷酸肌醇诱导的钙释放的途径而实现的,而胞外钙离子不参与这一过程。
AIM: To investigate the role of intracellular calcium mobilization in calcium-sensitive potassium currents (I (K (Ca))) in the gastric smooth muscle cells of the gastric antrum in rats treated with sodium nitroprusside (SNP) .Methods: Single cell acute myeloid leukemia was induced by collagenase, and sodium nitroprusside was used as a nitric oxide donor.Results: SNP at 100 μmol / L significantly increased calcium-sensitive potassium current and significantly increased transient outward potassium current (STOC) The increasing effect of I_ (K (Ca)) could not be blocked by extracellular calcium-free solution (containing 10 μmol / L of etidronate) and 5 μmol / L of L-type calcium channel blocker nicardipine.SNP100 μmol / L Can significantly inhibit the calcium current.SNP-induced STOC increased significantly by the inositol triphosphate receptor specific blocking heparin 3g / L blocked, but can not be blocked by ranitidine 10μmol / L. Methylene blue 1 μmol / L, specific intracellular guanylate cyclase inhibitor, can also significantly inhibit the above effects.Conclusion: SNP-induced calcium-sensitive potassium current may be increased by intracellular cGMP Inositol triphosphate-induced calcium release pathway is achieved, while extracellular calcium is not involved in this process.