Potassium channels regulate cholecystokinin secretion in STC-1 cells.
Following blockade of plasma membrane potassium channels with barium or tetraethylammonium chloride, release of cholecystokinin was increased in an intestinal cell line (STC-1). Treatment with calcium channel blockers inhibited barium- or TEA-induced secretion. Barium chloride also stimulated 45Ca efflux from STC-1 cells. Whole cell patch clamp recordings revealed a voltage-activated, L-type calcium current. We conclude that, inhibition of basally active potassium channels may depolarize STC-1 cells, producing activation of voltage-gated calcium influx pathways. Influx of calcium may lead to a release of intracellular calcium which stimulates cholecystokinin secretion.
Snow
N D
ND
Department of Medicine, Duke University Medical Center, Durham, NC 27710.
Mangel
A W
AW
Sharara
A I
AI
Liddle
R A
RA
D001464:Barium / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism; D002460:Cell Line; D002766:Cholecystokinin / Q000378:metabolism*; D004553:Electric Conductivity; D007413:Intestinal Mucosa / Q000378:metabolism*; D009529:Nicardipine / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D001464:Barium; D019789:Tetraethylammonium; D002766:Cholecystokinin; D009529:Nicardipine; D002118:Calcium