FIGURE 3.

Cellular components that control gastric acid secretion. Numerous cell types regulate gastric acid secretion. Enterochromaffin-like (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 enteric nervous system (ENS) stimulates G cells through gastrin-releasing peptide (GRP) and acetylcholine (ACh) and stimulates ECL cells through pituitary adenylate cyclase-activating peptide (PACAP). The cholinergic signal can also inhibit somatostatin release from D cells, accelerating acid secretion. Additionally, calcitonin gene-related peptide (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.