The acid-secretingoxyntic cell, or parietal cell,
I is the main cell type in the gastric gland. Chief , cells (pepsinogen-secretingcells), mucus cells, s and D-cells (somatostatin-secreting cells) are also found within gastric glands. Somatostatin, released from fundic D-cells, inhibits the release of acid secretion from the parietal cell. These specialized cells are in close proximity to parasympathic nerve endings and neural inputs are able to regulate hormone release (10).The release of HA from enterochromaf-fin-like (ECL) cells can also be neurally mediated and subsequently stimulates parietal cells to secrete acid. Vagal nerve stimulation initiates the release of gastrin from antral G-cells, and acetylcholine (Ach) from postganglionic, cholinergic, and muscarinic nerves, which bind to their respective receptors on the ECL-cell to release HA. and subsequently acid from parietal cells (Fig. 3.2).
Ach, HA, and gastrin stimulate acid secretion by activating specific receptors on the ba-solateral membrane of the parietal cell. Once bound to the respective G-protein-coupled receptor, second-messenger systems are activated. Ach and gastrin activate phospholipase C to catalyze the conversion of membrane-bound phospholipids to diacylglycerol and inositol triphosphate. The release of Ca2+ from intracellular stores and the subsequent increase in cytoplasmic Ca2+ activates H+/K+-(proton pump). The binding of HA to the H2-receptor activates adenylate cyclase, resulting in an increase in cAMP, which activates the proton pump (11).
Many peptides and neurotransmitters have been identified as having a direct or indirect effect on the parietal cell. Somatostatin, secre-
Figure 3.2. Stimulation of acid secretion from the parietal cell.
Histamine tin, and prostaglandin E reduce acid secretion either indirectly, by inhibiting the release of gastrin, or directly, by an action at the parietal cell (12). Interleukins, vasoactive intestinal peptide, cholecystokinin (CCK), calcitonin gene-related peptide, oxyntomodulin, neurotensin, adrenaline, and gastric inhibitory polypeptide may inhibit parietal cell secretion indirectly through the release of local somatostatin. Peptide YY, CCK, and 5-HT are thought to influence acid secretion by modulating neural tone to the stomach. The release of nitric oxide release may also inhibit gastric acid secretion.
In addition to mucus from goblet cells, bicarbonate ions are secreted from the stomach to protect the gastric mucosa from gastric acid. Bicarbonate secretion occurs when the luminal pH is less than 2 and its release is regulated both neuronally and hormonally.
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