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Gastric Enterochromaffin-Like Cells and the Regulation of Acid Secretion

George Sachs, Christian Prinz

Open publisher page 12 citations

Abstract

The interaction of gastrin, somatostatin, and other transmitters at the level of the histamine-containing enterochromaffin (ECL) cell is the major pathway determining rate of gastric acid secretion. Gastrin stimulates ECL cell elevation of [Ca2+]i, synthesis of histidine decarboxylase, histamine release, and cell growth by binding at a cholecystokinin-B receptor. Somatostatin inhibits gastrin-dependent elevation of [Ca2+]i and hence histamine release by binding to stomatostatin receptor 2 subtype.

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What this paper is about

The interaction of gastrin, somatostatin, and other transmitters at the level of the histamine-containing enterochromaffin (ECL) cell is the major pathway determining rate of gastric acid secretion. Gastrin stimulates ECL cell elevation of [Ca2+]i, synthesis of histidine decarboxylase, histamine release, and cell growth by binding at a cholecystokinin-B receptor. Somatostatin inhibits gastrin-dependent elevation of [Ca2+]i and hence histamine release by binding to stomatostatin receptor 2 subtype.

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OpenAlex reports 12 citations for this work. Citation counts describe recorded attention and do not establish research quality.

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Available abstract

The interaction of gastrin, somatostatin, and other transmitters at the level of the histamine-containing enterochromaffin (ECL) cell is the major pathway determining rate of gastric acid secretion. Gastrin stimulates ECL cell elevation of [Ca2+]i, synthesis of histidine decarboxylase, histamine release, and cell growth by binding at a cholecystokinin-B receptor. Somatostatin inhibits gastrin-dependent elevation of [Ca2+]i and hence histamine release by binding to stomatostatin receptor 2 subtype.

Key concepts: Gastrin, Enterochromaffin-like cell, Enterochromaffin cell, Histidine decarboxylase, Histamine, Somatostatin, Secretion, Gastric acid

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