Regulation of cholecystokinin secretion by ATP-sensitive potassium channels.
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 86Rb efflux studies showed that an ATP-sensitive potassium channel was endogenously expressed in STC-1 cells. Furthermore, channels are present in sufficient number to significantly modulate whole cell potassium permeability after either channel activation or closure with diazoxide (100 microM) or disopyramide (200 microM), 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 microM). 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.
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Related Subject Headings
- Rubidium
- Potassium Channels
- Membrane Potentials
- Intestinal Mucosa
- Electrophysiology
- Cytosol
- Cholecystokinin
- Cell Line
- Cardiovascular System & Hematology
- Calcium
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Rubidium
- Potassium Channels
- Membrane Potentials
- Intestinal Mucosa
- Electrophysiology
- Cytosol
- Cholecystokinin
- Cell Line
- Cardiovascular System & Hematology
- Calcium