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为探讨生长抑素抑制胰岛素分泌的分子机制，我们以ＨＩＴ细胞为模型进行体外实验，系统全面地探讨了其对胰岛素分泌、钙离子跨膜电流、细胞内钙离子浓度、细胞内钾离子外流以及ＨＩＴ细胞腺苷酸环化酶和ｃＡＭＰ水平的影响。发现生长抑素能在不影响ＨＩＴ细胞腺苷酸环化作用以及细胞内外钾离子分布的情况下剂量依赖性地抑制细胞胰岛素的分泌，同时伴有钙离子跨膜流动和细胞内钙离子水平的升高。百日咳毒素可拮抗生长抑素的这种抑制作用。这些资料表明，抑制细胞外钙离子通过百日咳毒素敏感性的Ｇ－蛋白调节的电压依赖性钙离子通道进入胰岛素分泌细胞，是生长抑素抑制胰岛素分泌的重要分子机制之一。
In order to explore the molecular mechanism of somatostatin inhibit insulin secretion, we in vitro experiments using HIT cells as a model, a comprehensive study of its effects on insulin secretion, calcium transmembrane current, intracellular calcium concentration, intracellular potassium outflow and HIT cellular adenylate cyclase and cAMP levels. Found that somatostatin can inhibit the secretion of cellular insulin in a dose-dependent manner without affecting the adenylate cyclability of HIT cells and the distribution of extracellular and extracellular potassium ions, accompanied by the transmembrane flux of calcium ions and the intracellular calcium level Rise. Pertussis toxin antagonizes this inhibitory effect of somatostatin. These data indicate that inhibition of extracellular calcium ion entry into insulin-secreting cells via pertussis toxin-sensitive G-protein-regulated voltage-dependent calcium channels is one of the important molecular mechanisms by which somatostatin suppresses insulin secretion.