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目的:观察氯通道阻断剂氟灭酸(NFA)对耳蜗螺旋动脉平滑肌细胞膜电位和电刺激血管周围交感神经纤维引起兴奋性接头电位(EJP)的影响。方法:在耳蜗螺旋动脉平滑肌离体标本上,运用细胞内微电极记录技术研究非甾体类抗炎药物对平滑肌细胞的作用。结果:100μmol/L NFA引起低静息膜电位平滑肌细胞产生了(14.7±4.4)mV的超极化反应,引起高静息膜电位平滑肌细胞仅产生了(1.4±0.8)mV的超极化反应(P<0.01)。NFA引起低静息膜电位平滑肌细胞的反应是浓度依赖性的,这一超极化反应能被钙激活钾通道的阻断剂北非蝎毒素(charybdotoxin)和iberiotoxin阻断。另外,在高静息膜电位的平滑肌细胞,NFA对刺激引起的平滑肌细胞EJP有更明显的抑制作用(P<0.01),但对低静息膜电位的平滑肌细胞引起的EJP作用不明显(P>0.05)。结论:NFA既能通过阻断钙激活的氯通道抑制平滑肌细胞产生的EJP,又能激活钙激活钾通道使平滑肌细胞产生超极化反应,表现出对平滑肌细胞作用的多样性。
AIM: To observe the effects of fluvastifluoride (NFA), a chloride channel blocker, on the membrane potential of the smooth muscle cells in the cochlear spiral arteries and the excitatory joint potentials (EJP) induced by electrical stimulation of perivascular sympathetic nerve fibers. Methods: The effects of NSAIDs on smooth muscle cells were studied by using intracellular microelectrode recording technique on isolated specimens of smooth muscle of cochlear spiral arteries. Results: Hyperlipidemia was induced in the low resting membrane potential smooth muscle cells by 100 μmol / L NFA for (14.7 ± 4.4) mV, resulting in hyperpolarization of (1.4 ± 0.8) mV in high resting membrane potential smooth muscle cells (P <0.01). The response of NFA to low resting membrane potential smooth muscle cells is concentration-dependent, and this hyperpolarization can be blocked by the chalnotoxin and iberiotoxin, a blocker of calcium-activated potassium channels. In addition, NFA inhibited EJP-induced smooth muscle cells more significantly (P <0.01) in smooth muscle cells with high resting membrane potential but not with EJP in smooth muscle cells at low resting membrane potential (P > 0.05). Conclusion: NFA not only can inhibit the EJP produced by smooth muscle cells by blocking the calcium-activated chloride channels, but also activate the calcium-activated potassium channels to induce hyperpolarization in smooth muscle cells and show the diversity of smooth muscle cells.