Malaisse W J, Sener A, Malaisse-Lagae F
Res Commun Chem Pathol Pharmacol. 1985 Jul;49(1):71-83.
The organic calcium-agonist CGP 28392 augmented insulin release evoked by D-glucose in rat pancreatic islets incubated in the presence or absence of gliclazide, but failed to stimulate insulin secretion in the absence of glucose or presence of diazoxide. Gliclazide, however, failed to augment insulin release evoked, in the presence of CGP 28392, by a high concentration of glucose (11.1 mM), and protected the B-cell against the inhibitory action of diazoxide. As judged from the relative magnitude of changes in 45Ca fractional outflow rate from prelabelled islets perifused at an intermediate glucose concentration (7.0 mM), CGP 28392 failed to affect the rapid cationic response to gliclazide, whereas this hypoglycemic sulfonylurea decreased the cationic response to CGP 28392. These results suggest that the functional response to gliclazide is attributable to a molecular mechanism distinct from the prolongation of the open time of calcium channels presumably provoked by the dihydropyridine.
有机钙激动剂CGP 28392在有或没有格列齐特存在的情况下，增强了D-葡萄糖诱导的大鼠胰岛胰岛素释放，但在无葡萄糖或有二氮嗪存在时未能刺激胰岛素分泌。然而，格列齐特在有CGP 28392存在时，未能增强高浓度葡萄糖（11.1 mM）诱导的胰岛素释放，并保护β细胞免受二氮嗪的抑制作用。根据在中等葡萄糖浓度（7.0 mM）下灌流的预先标记胰岛中45Ca分数流出率变化的相对幅度判断，CGP 28392未能影响对格列齐特的快速阳离子反应，而这种降血糖磺酰脲降低了对CGP 28392的阳离子反应。这些结果表明，对格列齐特的功能反应归因于一种与二氢吡啶可能引发的钙通道开放时间延长不同的分子机制。
