胃腺壁细胞钙信号的调节

Regulation of parietal cell calcium signaling in gastric glands.

作者信息

Athmann C, Zeng N, Scott D R, Sachs G

机构信息

Department of Physiology, University of California, Los Angeles, West Los Angeles Healthcare Center, Los Angeles, California 90073, USA.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2000 Nov;279(5):G1048-58. doi: 10.1152/ajpgi.2000.279.5.G1048.

DOI:10.1152/ajpgi.2000.279.5.G1048

PMID:11053003

Abstract

The ligands interacting with enterochromaffin-like (ECL) and parietal cells and the signaling interactions between these cells were investigated in rabbit gastric glands using confocal microscopy. Intracellular calcium concentration (Ca(2+)) changes were used to monitor cellular responses. Histamine and carbachol increased Ca(2+) in parietal cells. Gastrin (1 nM) increased Ca(2+) in ECL cells and adjacent parietal cells. Only the increase of Ca(2+) in parietal cells was inhibited by H(2) receptor antagonists (H(2)RA). Gastrin (10 nM) evoked an H(2)RA-insensitive Ca(2+) increase in parietal cells. Carbachol produced large H(2)RA- and somatostatin-insensitive signals in parietal cells. Pituitary adenylate cyclase-activating peptide (PACAP, 100 nM) elevated Ca(2+) in ECL cells and adjacent parietal cells. H(2)RAs abolished the PACAP-stimulated Ca(2+) increase in adjacent parietal cells. Somatostatin did not inhibit the increase of Ca(2+) in parietal cells stimulated with histamine, high gastrin concentrations, or carbachol but abolished ECL cell calcium responses to gastrin or PACAP. Hence, rabbit parietal cells express histaminergic, muscarinic, and CCK-B receptors coupled to calcium signaling but insensitive to somatostatin, whereas rabbit and rat ECL cells express PACAP and CCK-B calcium coupled receptors sensitive to somatostatin.

摘要

利用共聚焦显微镜在兔胃腺中研究了与肠嗜铬样（ECL）细胞和壁细胞相互作用的配体以及这些细胞之间的信号相互作用。细胞内钙浓度（Ca(2+)）变化用于监测细胞反应。组胺和卡巴胆碱可增加壁细胞中的Ca(2+)。胃泌素（1 nM）可增加ECL细胞和相邻壁细胞中的Ca(2+)。只有壁细胞中Ca(2+)的增加可被H(2)受体拮抗剂（H(2)RA）抑制。胃泌素（10 nM）可引起壁细胞中对H(2)RA不敏感的Ca(2+)增加。卡巴胆碱在壁细胞中产生对H(2)RA和生长抑素不敏感的大信号。垂体腺苷酸环化酶激活肽（PACAP，100 nM）可提高ECL细胞和相邻壁细胞中的Ca(2+)。H(2)RAs消除了PACAP刺激的相邻壁细胞中Ca(2+)的增加。生长抑素不抑制组胺、高浓度胃泌素或卡巴胆碱刺激的壁细胞中Ca(2+)的增加，但消除了ECL细胞对胃泌素或PACAP的钙反应。因此，兔壁细胞表达与钙信号传导偶联但对生长抑素不敏感的组胺能、毒蕈碱能和CCK-B受体，而兔和大鼠ECL细胞表达对生长抑素敏感的PACAP和CCK-B钙偶联受体。