Enterochromaffin-like cells stimulation

Histamine (B). Histamine is stored in basophils and tissue mast cells. It plays a role in inflammatory and allergic reactions (p. 72, 326) and produces bronchoconstriction, increased intestinal peristalsis, and dilation and increased permeability of small blood vessels. In the gastric mucosa, it is released from enterochromaffin-like cells and stimulates acid secretion by the parietal cells. In the CNS, it acts as a neuromodulator. Two receptor subtypes (G-pro-tein-coupled), H and H2. are of therapeutic importance both mediate vascular responses. Prejunctional H3 receptors exist in brain and the periphery. 

The stomach secretes hydrochloric acid under the influences of vagus nerve stimulation, gastrin and histamine. Histamine is the most potent stimulus of gastric acid secretion in some animal species studied, such as the horse (Kitchen et al 1998a). Histamine is released by mast cells and enterochromaffin-like cells that are immediately adjacent to the parietal cells. Histamine interacts with two distinct subsets of histamine H2 receptors on the parietal cell membrane, initiating a series of reactions that result in the phosphorylation of protein kinases and increased intracellular calcium within the parietal cell. This, in turn, results in transformation and translocation of the... 

Mast cells and enterochromaffin-like cells found in the interstitium and among parietal cells contain histamine, which acts on parietal cell receptors to stimulate the release of hydrochloric acid. The histamine receptor on parietal cells is designated as H2 and is blocked by H2 blockers such as cimetidine which are widely used to treat peptic ulcers. 

Ryber B, Tielemanns Y, Axelson J, et al. Gastrin stimulates the self-replication of enterochromaffin-like cells in the rat stomach. Gastroenterology 1990 99 935. 

In close proximity to the parietal cells are gut endocrine cells called enterochromaffin-like (ECL) cells. ECL cells also have receptors for gastrin and acetylcholine, which stimulate histamine release. Histamine binds to the H2 receptor on the parietal cell, resulting in activation of adenylyl cyclase, which increases intracellular cyclic adenosine... 

Histamine from nearby enterochromaffin-like (ECL) cells is probably the primary modulator, but the magnitude of the stimulus depends upon an interaction of signals of each type low levels of only histamine or gastrin weakly stimulate acid secretion, but together they strongly reinforce it. Pharmacologic antagonists of each of these molecules can block acid secretion. 

Figure 4.2 Gastric add production. Two cell types in the mucosa of the corpus of stomach are principally responsible for secretion of acid. Histamine secreted from nearby enterochromaffin-like (ECL) cells stimulates parietal cells to secrete acid. A variety of substances can stimulate the ECL cell to secrete histamine, including PCAP, pituitary adenyl cyclase-activab ng peptide (released from enteric nervous system interneurones in the gastric mucosa), and gastrin, both stimulating ECL cells via adenyl cyclase to raise intracellular levels of cAMP that lead to histamine secretion.

Stimulation of parietal cells for gastric acid secretion is a complex process mediated both centrally by vagal parasympathic fibers and peripherically by release of histamine from the fundic mucosal enterochromaffin-like... 

Stimulation of acid secretion by the parietal cell is due mainly to gastrin-or pituary adenylate cyclase activating peptide (PACAP)-stimulated release of histamine from the enterochromaffin-like (ECL) cell of the fundic epithelium and activation of the H2 receptor. Direct stimulation by acetylcholine occurs at an M3 receptor on the parietal cell. The parietal cell also has a cholecystokinin B (CCK-B) receptor which appears to require permissive activation of the H2 receptor for elevation of parietal cell calcium. The H2 receptor is coupled to mainly Gs with elevation of cAMP but also to Gq, resulting in a small stimulation of intracellular calcium levels. The final event is activation of the H,K ATPase, which is in a resting, nonsecreting state in cytoplasmic membranes [24-26]. 

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