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(Icch)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Icch的变化.结果:低渗性膜牵张明显增强Icch;Icch阻断剂奎尼丁3μmol/L完全抑制Icch和低渗膜牵张引起的Icch增强效应;胞外无钙状态下低渗膜牵张引起的Icch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100nmol/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Icch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Icch增强效应.结论:低渗性膜牵张增强Icch,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.%AIM: To investigate the role of intracellular calcium in muscarinic currents increased by hypoosmotic membranestretch in gastric antral circular myocytes of the guinea pig. METHODS: The whole cell patch-clamp techniquewas used, and the myocytes were isolated by collagenase. Cells were swelled by hypoosmotic solution (200Osmmol/kg). RESULTS: The hypoosmotic membrane stretch markedly increased carbachol-induced muscariniccurrents (Icch). The Icch and the increase of Icch were completely blocked by quinidine 3μmol/L, a specific musca-rinic current blocker. In external calcium-free solution hypoosmotic membrane stretch could not increaseICCh, butin the presence of nicadipine 5 μmol/L, a L-type calcium channel blocker or gadolinium chloride 100 nmol/L, astretch-activated cation channel blocker, theIcch was still increased by hypoosmotic membrane stretch. When bothnicardipine and gadolinium chloride were added into external solution,Icch were not increased by hypoosmoticmembrane stretch any more. Ryanodine, a calcium-induced calcium release (CICR) agonist completely blockedhypoosmotic membrane stretch-induced increase of Icch@ CONCLUSION: Hypoosmotic membrane stretch in-creased Icch and the increment was related to influx of external calcium and CICR.
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