Shibuya I, Kanno T
Am J Physiol. 1985 Mar;248(3 Pt 1):C228-34. doi: 10.1152/ajpcell.1985.248.3.C228.
Continuous stimulation with 8 pM cholecystokinin octapeptide (CCK-8) induced a gradual increase in pancreatic protein output and little if any change in redox state of cytochromes aa3, b, and c + c1. The protein output was completely abolished when CaCl2 was removed from the perfusing and bathing solution. Continuous stimulation with 200 pM CCK-8 induced the rapid and largest protein output and a distinct reduction of cytochromes and nicotinamide nucleotides. These responses were partially decreased in the Ca2+-deficient environment and enhanced immediately after the replacement with the standard solution. These and other results are compatible with the view that reduction of electron transfer system in the pancreatic acinar cell may be induced by stimulation with the secretagogue in pharmacological concentration and that the reduction may coincide with uptake and retention of cytoplasmic excess Ca2+ by mitochondria.
用8皮摩尔胆囊收缩素八肽（CCK - 8）持续刺激可使胰腺蛋白输出逐渐增加，而细胞色素aa3、b和c + c1的氧化还原状态几乎没有变化。当从灌注液和浴液中去除氯化钙时，蛋白输出完全消失。用200皮摩尔CCK - 8持续刺激可诱导快速且最大的蛋白输出以及细胞色素和烟酰胺核苷酸明显减少。在缺钙环境中这些反应部分减弱，而在用标准溶液替换后立即增强。这些及其他结果与以下观点相符，即药理学浓度的促分泌素刺激可能诱导胰腺腺泡细胞中电子传递系统的还原，且这种还原可能与线粒体对细胞质中过量Ca2+的摄取和潴留同时发生。
