Effect of somatostatin and calcium deprivation on cholecystokinin or caerulein-induced insulin and glucagon release from the isolated perfused rat pancreas.

The present experiments were undertaken to investigate the effect of alteration in on extracellular calcium concentration and of somatostatin on cholecystokinin-(CCK)- and caerulein-induced insulin and glucagon release from the isolated perfused rat pancreas. In control studies using perfusate containing 2.5 mM CaCl2 and 50 mg/dl glucose, CCK and caerulein caused insulin and glucagon release in a dose-related fashion. During perfusion with calcium free medium, insulin release was markedly inhibited. Subsequent introduction of 2.5 mM CaCl2 to the medium restored insulin response toward control levels. Extracellular calcium depletion, however, had no effect on CCK- or caerulein-induced glucagon release. The output of glucagon in the absence of calcium was comparable to that seen in the control experiments. On the other hand, somatostatin abolished the increase in glucagon secretion, but not the increase in insulin secretion, when perfused simultaneously with CCK or caerulein. However, pretreatment for 10 min with somatostatin blocked even insulin secretion. However, pretreatment for 10 min with somatostatin blocked even insulin secretion. The effects of somatostatin on hormonal discharge are suggested to be related to an alteration in the handling of or response to calcium. Recently, somatostatin has also been shown to inhibit calcium uptake by islets. Thus, the present results indicate a differential sensitivity of CCK- and caerulein-stimulated alpha and beta cell to extracellular calcium depletion and to the effect of somatostatin.