Calcium-dependent secretory and redox response to CCK-8 in isolated perfused rat pancreas

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.