PHENYLALANINE-STIMULATED SECRETION OF CHOLECYSTOKININ IS CALCIUM-DEPENDENT
Mangel, A., PRPIC, V., WONG, H., BASAVAPPA, S., HURST, LJ., SCOTT, L., GARMAN, RL., HAYES, JS., SHARARA, AI., SNOW, ND., WALSH, JH., & LIDDLE, RA. (1995). PHENYLALANINE-STIMULATED SECRETION OF CHOLECYSTOKININ IS CALCIUM-DEPENDENT. American Journal of Physiology. Gastrointestinal and Liver Physiology, 268(1), G90-G94.
The secretion of cholecystokinin was examined in STC-1 cells, an intestinal cholecystokinin (CCK)secreting cell line. Exposure to the amino acid L-phenylalanine increased release of CCK by 135%, 180%, and 251% of control levels after 15-min treatments with 5, 20, and 50 mM phenylalanine, respectively. L-Phenylalanine-induced secretion of CCK was inhibited by the calcium channel blocker diltiazem (10 mu M). L-Phenylalanine (20 mM) also significantly increased cytosolic calcium levels in fura 2-acetoxymethyl ester (fura 2-AM)-loaded cells, and this increase was diltiazem sensitive. D-Phenylalanine, over the dose range of 5-50 mM, produced nonsignificant increases in CCK release. Treatment of STC-1 cells with 300 ng/ml of pertussis toxin for either 4 or 24 h did not significantly affect either basal release of CCK or L-phenylalanine-stimulated secretion. Patch-clamp recordings from cell-attached membrane patches showed a stimulation in calcium channel activity after L-phenylalanine. These results indicate that, in STC-1 cells, L-phenylalanine stimulates release of cholecystokinin via a calcium-dependent process.