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Cellular components that control gastric acid secretion

Cellular components that control gastric acid secretion
Cellular components that control gastric acid secretion. Numerous cell types regulate gastric acid secretion. ECL cells through histamine and X cells that secrete ghrelin activate parietal cells via paracrine and neural pathways, respectively. Gastrin secreted from G cells binds directly on parietal cells or stimulates acid secretion mediated by histamine release from ECL cells. Vagal efferent mediated by the ENS stimulates G cells through GRP and ACh and stimulates ECL cells through PACAP. The cholinergic signal can also inhibit somatostatin release from D cells, accelerating acid secretion. Additionally, CGRP released from vagal afferent terminals activates X cells to enhance the acid secretory pathway. Somatostatin directly inhibits gastric acid secretion from parietal cells as well as indirectly through its action on ECL cells and G cells. Histamine suppresses ECL cell activity as a negative feedback system. Apelin, produced by parietal cells, exerts inhibitory or stimulatory effects on ECL cells.
PACAP: pituitary adenylate cyclase-activating peptide; ECL: enterochromaffin-like; GRP: gastrin-releasing peptide; ENS: enteric nervous system; CGRP: calcitonin gene-related peptide; ACh: acetylcholine.
Reproduced with permission from: Engevik AC, Kaji I, Goldenring JR. The physiology of the gastric parietal cell. Physiol Rev 2020; 100:573. Copyright © 2021 American Physiological Society.
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