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Wadsworth Veterans Affairs Hospital, Los Angeles, California 90073
Peptides release histamine from enterochromaffin-like (ECL)
cells because of elevation of intracellular Ca2+
concentration ([Ca2+]i) by either
receptor-operated or voltage-dependent Ca2+ channels
(VDCC). To determine whether VDCCs contribute to histamine release
stimulated by gastrin or pituitary adenylate cyclase-activating polypeptide (PACAP), the presence of VDCCs and their possible modulation by peptides was investigated in a 48-h cultured rat gastric
cell population containing 85% ECL cells. Video imaging of fura
2-loaded cells was used to measure
[Ca2+]i, and histamine was assayed
by RIA. Cells were depolarized by increasing extracellular
K+ concentrations or by 20 mM
tetraethylammonium (TEA+). Cell depolarization increased
transient and steady-state [Ca2+]i
and resulted in histamine release, dependent on extracellular Ca2+. These K+- or TEA+-dependent
effects on histamine release from ECL cells were coupled to activation
of parietal cells in intact rabbit gastric glands, and L-type channel
blockade by 2 µM nifedipine inhibited 50% of [Ca2+]i elevation and histamine
release. N-type channel blockade by 1 µM 
-conotoxin GVIA inhibited
25% of [Ca2+]i elevation and 14%
of histamine release. Inhibition was additive. The effects of 20 mM
TEA+ were fully inhibited by 2 µM nifedipine. Both
classes of Ca2+ channels were found in ECL cells, but not
in parietal cells, by RT-PCR. Nifedipine reduced PACAP-induced (but not
gastrin-stimulated) Ca2+ entry and histamine release by
40%. Somatostatin, peptide YY (PYY), and galanin dose
dependently inhibited L-type Ca2+ channels via a pertussis
toxin-sensitive pathway. L-type VDCCs play a role in PACAP but not
gastrin stimulation of histamine release from ECL cells, and the
channel opening is inhibited by somatostatin, PYY, and galanin by
interaction with a Gi or Go protein.
acid secretion; gastric glands; calcium channels
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