Electrophysiology of intestinal cholecystokinin secretion.
The control of gastrointestinal CCK secretion may occur at several points. A decrease in potassium conductance may depolarize the plasma membrane, activating calcium channels with a resultant stimulation in CCK release. The opposite may occur with increases in potassium conductance. The model presented in Fig. 8 suggests that the key control point in the understanding of CCK secretion is the regulation of L-type calcium channels. Whether a single second messenger pathway may regulate calcium channels stimulated by agents such as glucose, phenylalanine, bombesin and cAMP is an important area to pursue.
Mangel
A W
AW
Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D015220:Calcium Channels / Q000378:metabolism; D002460:Cell Line; D002766:Cholecystokinin / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism*; D008564:Membrane Potentials; D010649:Phenylalanine / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism
D015220:Calcium Channels; D015221:Potassium Channels; D010649:Phenylalanine; D000255:Adenosine Triphosphate; D002766:Cholecystokinin; D000242:Cyclic AMP