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目的和方法：采用分离的Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠心室肌细胞，以Ｆｕｒａ－２／ＡＭ荧光指示剂负载，检测心肌细胞内游离钙浓度（［Ｃａ２＋］ｉ）变化，探讨内皮素－１（ＥＴ－１）对［Ｃａ２＋］ｉ的作用及其机制。结果：ＥＴ－１（１×１０－７ｍｏｌ／Ｌ）引起［Ｃａ２＋］ｉ升高分两个时相：快速相和持续相，可被ＥＴＡ的特异性受体阻断剂ＢＱ１２３（２×１０－６ｍｏｌ／Ｌ）所阻断。移去细胞外液钙以及用百日咳毒素（２００ｎｇ／ｍＬ）处理１０ｈ后，ＥＴ－１仍引起快速相，但持续相消失。Ｒｙａｎｏｄｉｎｅ（４μｍｏｌ／Ｌ）和异搏定（２×１０－５ｍｏｌ／Ｌ）对ＥＴ－１诱导［Ｃａ２＋］ｉ升高的作用无显著影响。结论：ＥＴ－１升高［Ｃａ２＋］ｉ是通过ＥＴＡ受体介导；快速相［Ｃａ２＋］ｉ升高主要由胞内Ｒｙａｎｏｄｉｎｅ不敏感的钙池释放造成，与百日咳毒素敏感的Ｇ蛋白无关；持续相［Ｃａ２＋］ｉ升高主要由胞外Ｃａ２＋内流引起，不是通过电压依赖性Ｌ－型钙通道介导，与百日咳毒素敏感的Ｇ蛋白有关
Objective: To investigate the changes of intracellular free calcium concentration ([Ca2 +] i) in cardiomyocytes isolated from isolated Sprague-Dawley rat ventricular myocytes with Fura-2 / AM fluorescent indicator. 1) Effect on [Ca2 +] i and its mechanism. Results: The increase of [Ca2 +] i caused by ET-1 (1 × 10-7mol / L) was divided into two phases: rapid phase and continuous phase, which could be blocked by ETA specific antagonist BQ123 (2 × 10- 6mol / L) blocked. After removal of extracellular calcium and after 10 h treatment with pertussis toxin (200 ng / mL), ET-1 still caused a rapid phase but continued to disappear. Ryanodine (4μmol / L) and verapamil (2 × 10-5mol / L) had no significant effect on the increase of [Ca2 +] i induced by ET-1. CONCLUSION: Elevated ET-1 is mediated by ETA receptors. The increase in fast phase [Ca2 +] i is mainly caused by intracellular release of Ryanodine-insensitive calcium pool, independent of pertussis toxin-sensitive G protein. Phase [Ca2 +] i elevation is mainly caused by extracellular Ca2 + influx, not by voltage-dependent L-type calcium channel-mediated pertussis toxin-sensitive G protein