Open AccessCellular Localization of Cholecystokinin Receptors as the Molecular Basis of the Periperal Regulation of Acid Secretion
Author(s) -
Schmidt Wolfgang E.,
Schmitz Frank
Publication year - 2002
Publication title -
pharmacology & toxicology
Language(s) - English
Resource type - Journals
eISSN - 1600-0773
pISSN - 0901-9928
DOI - 10.1034/j.1600-0773.2002.910612.x
Subject(s) - gastrin , cholecystokinin , cholecystokinin receptor , gastric acid , receptor , medicine , enteroendocrine cell , endocrinology , secretion , g cell , histamine , regulation of gastric function , paracrine signalling , gastrointestinal hormone , pathogenesis , biology , endocrine system , peptide hormone , hormone
Gastrin stimulates gastric acid secretion through direct activation of CCK‐B/gastrin receptors on parietal cells and indirectly through release of histamine from ECL cells. Cholecystokinin (CCK) is structurally closely related to gastrin and shares high affinity for CCK‐B/gastrin receptors. In contrast to gastrin, CCK also recognizes CCK‐A receptors. While CCK appears to be a negative regulator of gastric acid secretion and postprandial release of gastrin in the normal human gastrointestinal tract, its impact on the pathogenesis of acid hypersecretion in Helicobacter pylori‐infected individuals remains uncertain. This article will review the endocrine and paracrine regulatory pathways which are activated by CCK/gastrin peptides and which appear relevant in the pathogenesis of peptic ulcer disease in man.