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目的:研究在低渗性膜牵张引起豚鼠胃窦环行肌细胞卡巴胆碱诱发的毒蕈碱受体门控电流(I_(CCh))增加过程中胞内钙的作用.方法:采用传统全细胞膜片箝技术,对以胶原酶急性分离的单细胞进行低渗灌流,观察I_(CCh)的变化.结果:低渗性膜牵张明显增强I_(CCh);I_(CCh)阻断剂奎尼丁3 μmol/L完全抑制I_(CCh)和 低渗膜牵张引起的I_(CCh)增强效应;胞外无钙状态下低渗膜牵张引起的I_(CCh)增强效应完全被抑制,但是单纯钙通道阻断剂尼卡地平5μmol/L或牵张刺激敏感阳离子通道阻断剂氯化钆100 nmol/L不能阻断;同时用尼卡地平和氯化钆处理能够完全阻断低渗膜牵张引起的I_(CCh)增强效应;用钙引发钙释放受体激动剂ryanodine处理也完全阻断低渗膜牵张引起的I_(CCh)增强效应.结论:低渗性膜牵张增强I_(CCh),这种增强效应与胞外钙进入胞内并诱发钙引起的钙库释放有关.
OBJECTIVE: To study the effect of intracellular calcium during cardiotachine-induced muscarinic receptor-gated currents (I_ (CCh)) induced by hypotonic membrane distraction in guinea-pig gastric antral myocytes.Methods: Cell patch clamp technique was used to observe the changes of I_ (CCh) in the single cells acutely isolated by collagenase.Results: I_ (CCh) The inhibitory effect of Ih (CCh) induced by I_ (CCh) and stretch at low permeation membrane was completely inhibited by 3 μmol / L of nimin. The enhancement of I_ (CCh) However, the simple calcium channel blocker nicardipine 5μmol / L or stretch-sensitive sensitive cationic channel blocker gadolinium chloride 100 nmol / L can not be blocked; at the same time with nicardipine and gadolinium chloride treatment can completely block the hypotonic (CCh) enhancement induced by membranous stretch.It also completely blocked I_ (CCh) enhancement induced by calcium-induced calcium release receptor agonist ryanodine.Conclusion: Hypotonic membrane stretch enhanced I_ (CCh), this enhancement effect and extracellular calcium into the intracellular Ca2 + -induced calcium release.