Mechanisms of intragastric pH sensing

被引：22

作者：

Goo T. ^{[1
,5
]}

Akiba Y. ^{[1
,2
,3
,4
]}

Kaunitz J.D. ^{[1
,2
,3
,4
]}

机构：

[1] Greater Los Angeles Veteran Affairs Healthcare System, West Los Angeles VA Medical Center, Building 114, Los Angeles, CA 90073

[2] Department of Medicine, UCLA School of Medicine, Los Angeles, CA

[3] CURE: Digestive Diseases Research Center, Los Angeles, CA

[4] Brentwood Biomedical Research Institute, Los Angeles, CA

[5] Cedars-Sinai Internal Medicine Residency, Los Angeles, CA

来源：

Current Gastroenterology Reports | 2010年 / 12卷 / 6期

基金：

美国国家卫生研究院;

关键词：

Acid-sensing ion channel; Amino acid; Calcitonin gene-related peptide; Calcium-sensing receptor; Gastrin; Parietal cell; G cell; D cell; Somatostatin; Transient receptor potential vanilloid subtype 1 (TRPV1);

D O I：

10.1007/s11894-010-0147-7

中图分类号：

学科分类号：

摘要：

Luminal amino acids and lack of luminal acidity as a result of acid neutralization by intragastric foodstuffs are powerful signals for acid secretion. Although the hormonal and neural pathways underlying this regulatory mechanism are well understood, the nature of the gastric luminal pH sensor has been enigmatic. In clinical studies, high pH, tryptic peptides, and luminal divalent metals (Ca2+ and Mg2+) increase gastrin release and acid production. The calcium-sensing receptor (CaSR), first described in the parathyroid gland but expressed on gastric G cells, is a logical candidate for the gastric acid sensor. Because CaSR ligands include amino acids and divalent metals, and because extracellular pH affects ligand binding in the pH range of the gastric content, its pH, metal, and nutrient-sensing functions are consistent with physiologic observations. The CaSR is thus an attractive candidate for the gastric luminal sensor that is part of the neuroendocrine negative regulatory loop for acid secretion. © 2010 The Author(s).

引用

页码：465 / 470

页数：5

共 37 条

[1]

Andersson S., Olbe L., Inhibition of gastric acid response to sham feeding in pavlov pouch dogs by acidification of antrum, Acta Physiol Scand, 61, pp. 55-64, (1964)

[2]

Barreras R.F., Calcium and gastric secretion, Gastroenterology, 64, pp. 1168-1184, (1973)

[3]

Behar J., Hitchings M., Smyth R.D., Calcium stimulation of gastrin and gastric acid secretion: effect of small doses of calcium carbonate, Gut, 18, 6, pp. 442-448, (1977)

[4]

Feurle G.E., Effect of rising intragastric pH induced by several antacids on serum gastrin concentrations in duodenal ulcer patients and in a control group, Gastroenterology, 68, pp. 1-7, (1975)

[5]

Mazzacca G., Cascione F., Budillon G., Et al., Parietal cell hyperplasia induced by long-term administration of antacids to rats, Gut, 19, pp. 798-801, (1978)

[6]

Schubert M.L., Peura D.A., Control of Gastric Acid Secretion in Health and Disease, Gastroenterology, 134, 7, pp. 1842-1860, (2008)

[7]

Shulkes A., Baldwin G.S., Giraud A.S., Regulation of gastric acid secretion, Physiology of the Gastrointestinal Tract, pp. 1223-1258, (2006)

[8]

Campos R.V., Buchan A.M., Meloche R.M., Et al., Gastrin secretion from human antral G cells in culture, Gastroenterology, 99, pp. 36-44, (1990)

[9]

Zeng N., Athmann C., Kang T., Et al., PACAP type i receptor activation regulates ECL cells and gastric acid secretion, J Clin Invest, 104, pp. 1383-1391, (1999)

[10]

Wank S.A., PACAP upsets stomach theory, J Clin Invest, 104, pp. 1341-1342, (1999)

← 1 2 3 4 →