Cellular localization of cholecystokinin receptors as the molecular basis of the periperal regulation of acid secretion.
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.
Schmidt
Wolfgang E
WE
Department of Medicine I at St. Josef-Hospital, Ruhr-University of Bochum, Gudrunstr. 56, D-44791 Bochum, Germany. wolfgang.e.schmidt@ruhr-uni-bochum.de
Schmitz
Frank
F
D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology; D005755:Gastrins / Q000502:physiology*; D006801:Humans; D008967:Molecular Biology; D010437:Peptic Ulcer / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D011949:Receptors, Cholecystokinin / Q000235:genetics / Q000378:metabolism / Q000502:physiology*
D005755:Gastrins; D011949:Receptors, Cholecystokinin