The acid-producing part of the stomach is rich in peptide-hormone-producing
endocrine/paracrine cells of different types. In birds and all mammals stu
died, ECL cells constitute the quantitatively predominant endocrine cell po
pulation in this location. They produce histamine and an as yet unidentifie
d peptide. hormone. The paracrine. action of the ECL cells is to provide hi
stamine to mediate the stimulating effect of gastrin on the acid-secreting
parietal cells: the gastrin-ECL cell-parietal cell axis.
Secretion of histamine from the ECL cells was studied in intact conscious r
ats subjected to gastric submucosal microdialysis and using isolated cells
in primary culture. The microdialysis experiments revealed that ECL-cell hi
stamine can be mobilized by the local infusion of gastrin, pituitary adenyl
ate cyclase-activating peptide (PACAP), vasoactive intestinal peptide (VIP)
, peptide YY (PYY), met-enkephalin, endothelin and noradrenaline/adrenaline
. While gastrin and met-enkephalin induced a sustained elevation of the sub
mucosal histamine concentration, endothelin, PYY, PACAP, VIP, and noradrena
line/adrenaline induced a transient elevation. Somatostatin, galanin and th
e prostanoid, misoprostol, inhibited gastrin-stimulated histamine mobilizat
ion. Studies of isolated ECL cells (80-90% purity) showed gastrin, PACAP an
d VIP to stimulate histamine secretion and somatostatin, galanin and misopr
ostol to inhibit gastrin-stimulated secretion. At present, it seems unlikel
y that metenkephalin, endothelin, adrenaline and PYY act directly on the EC
L cells in situ since the effects could not be reproduced with isolated ECL
cells. Clearly, the ECL cells operate under the multifactorial control of
circulating hormones, local hormones, catecholamines, neuropeptides and inf
lammatory mediators.