The relationship of potassium channel activity to the secretion of cholecystokinin (CCK) was evaluated in STC-1 cells, an intestinal CCK-secreting cell line. Patch-clamp and Rb-86 efflux studies showed that an ATP-sensitive potassium channel was endogenously expressed in STC-1 cells. Furthermore, chan nels are present in sufficient number to significantly modulate whole cell potassium permeability after either channel activation or closure with diazoxide (100 mu M) or disopyramide (200 mu M), respectively. Inhibition of channel activity with glucose (5-20 mM) was found to depolarize the plasma membrane, increase cytosolic calcium levels, and stimulate CCK release. Glucose-mediated release of CCK, as well as the increase in cytosolic calcium, was inhibited by the calcium channel blocker diltiazem (10 mu M). It is concluded that intestinal secretion of CCK may be tonically controlled by activity of basally active ATP-sensitive potassium channels, and after inhibition of channel activity, calcium-dependent CCK secretion is stimulated.
REGULATION OF CHOLECYSTOKININ SECRETION BY ATP-SENSITIVE POTASSIUM CHANNELS
Mangel, A., PRPIC, V., SNOW, ND., BASAVAPPA, S., HURST, LJ., SHARARA, AI., & LIDDLE, RA. (1994). REGULATION OF CHOLECYSTOKININ SECRETION BY ATP-SENSITIVE POTASSIUM CHANNELS. American Journal of Physiology. Gastrointestinal and Liver Physiology, 267(4), G595-G600.