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L-type calcium channels regulate gastrin release from human antral G cells
J M Ray1, P E Squires, R M Meloche
1Department of Physiology, University of British Columbia, Vancouver, Canada.
The American Journal of Physiology
|August 1, 1997
Summary
Human antral gastrin cells express L-type calcium channels (VDCCs) crucial for beta-adrenergic stimulated gastrin release. However, these channels are not the sole mechanism for calcium-mediated gastrin secretion.
Area of Science:
- Endocrinology
- Cell Physiology
- Molecular Biology
Background:
- Gastrin (G) cells regulate gastric acid secretion.
- The role of voltage-dependent calcium channels (VDCCs) in G cell function is not fully understood.
Purpose of the Study:
- To investigate the presence and function of L-type VDCCs in human antral G cells.
- To determine the role of these channels in mediating beta-adrenergic stimulated gastrin release.
Main Methods:
- RT-PCR to identify VDCC alpha 1-subunit mRNA in human antral cells.
- Immunohistochemistry using antibodies against class D alpha 1-subunit.
- Measurement of gastrin release and intracellular calcium in response to agonists and calcium channel blockers.
Main Results:
- Human antral G cells express mRNA for class C and D L-type VDCC alpha 1-subunits.
- Class D alpha 1-subunit is present on the surface of G cells.
- Blockade of L-type VDCCs abolished terbutaline- and forskolin-stimulated gastrin release, with partial reversal by high extracellular calcium.
- Nitrendipine reduced the rise in intracellular calcium in G cells upon increased extracellular calcium.
Conclusions:
- Human antral cells express functional class C and D L-type VDCCs.
- Extracellular calcium influx via L-type VDCCs is essential for beta-adrenergic stimulated gastrin release.
- L-type channel activation is not the sole pathway for calcium-stimulated gastrin release.