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内皮系-1（ET-1）是一种强的生长因子，并诱导心肌细胞肥大反应。在本实验中，我们探讨了G蛋白、蛋白激酶C（PKC）和Na＋－H＋交换在ET-1诱导的培养新生大鼠心肌细胞肥大反应中的作用。ET-1（10－10～10－7mol／L）促进3H－亮氨酸掺入，增加细胞蛋白质的含量和心肌细胞的表面积，且呈剂量依赖性，它们的EC50分别为5．2×10-10，5．2×10－10和7．3×10－10mol／L。用蛋白激酶C（PKC）抑制剂，Staurosporin（2nmol／L）预处理心肌细胞，可完全阻断ET-1诱导的心肌细胞的这些肥大反应，而蛋白激酶C激动剂，佛波酸酯（PMA）（10－8～10－6mol／L）呈剂量依赖性促进心肌细胞的肥大反应。用Na＋－H＋交换抑制剂，氨氯毗咪（10-4mol／L）预处理心肌细胞，可抑制ET－1诱导的心肌细胞肥大反应，但不影响PMA诱导的心肌细胞肥大反应。百日咳毒素（150ng／ml）预处理心肌细胞，可明显抑制ET－1诱导的心肌细胞肥大反应。这些结果提示，ET-1诱导的培养新生大鼠心肌细胞肥大反应是与百日咳毒素敏感的G蛋白相耦联，蛋白激酶C和Na＋．H＋交换可能在ET-1诱导的心肌细胞肥大反应中是重要的细胞内信使转导途径。
Endothelial-1 (ET-1) is a strong growth factor and induces cardiomyocyte hypertrophy. In this experiment, we explored the role of G protein, protein kinase C (PKC) and Na + -H + exchange in ET-1-induced cardiomyocyte hypertrophy in cultured neonatal rats. ET-1 (10-10 ~ 10-7mol / L) promoted 3H-leucine incorporation, increased cell protein content and surface area of cardiomyocytes in a dose-dependent manner with EC50 of 5.2 × 10 -10, 5.2 × 10 -10 and 7.3 × 10 -10 mol / L. Pretreatment of cardiomyocytes with a protein kinase C (PKC) inhibitor, Staurosporin (2 nmol / L) completely blocked these hypertrophic responses by ET-1-induced cardiomyocytes, whereas protein kinase C agonists, ) (10-8 ~ 10-6mol / L) promoted the hypertrophic response of cardiomyocytes in a dose-dependent manner. Pretreatment of cardiomyocytes with Na + -H + exchange inhibitor and amlodipine (10-4mol / L) inhibited cardiomyocyte hypertrophy induced by ET-1 but did not affect PMA-induced cardiomyocyte hypertrophy. Pretreatment of cardiomyocytes with pertussis toxin (150 ng / ml) significantly inhibited cardiomyocyte hypertrophy induced by ET-1. These results suggest that the cardiomyocyte hypertrophy induced by ET-1 in cultured neonatal rat is coupled with pertussis toxin-sensitive G protein, protein kinase C and Na +. H + exchange may be an important intracellular messenger transduction pathway in ET-1-induced cardiomyocyte hypertrophy.