@article{aca7a9ae183b493a91cfcdb74a38e09c,
title = "Pentagastrin selectively modulates levels of mRNAs encoding apical H/K adenosine triphosphatase and basolateral Na-K-Cl cotransporter in rat gastric fundic mucosa",
abstract = "Background. Gastrin regulates gastric acid secretion and gastric mucosal cell proliferation. We hypothesized that pentagastrin administration would affect mRNA levels of two membrane proteins that are important during stimulated states of HC1 secretion, the basolateral Na-K-C1 cotransporter (BSC) and the apical H/K adenosine triphosphatase (H/K). Methods. Two groups of Fischer rats received intraperitoneal injections of pentagastrin (2.5 or 25 μg/kg) every 8 hours for three doses. A third group served as controls. An additional group received pentagastrin plus the gastrin receptor antagonist (GRA) L740,093. Fundic mucosae were subjected to semiquantitative Northern analysis of mRNAs encoding H/K and BSC. The mRNA for Na/K adenosine triphosphatase (Na/K), a transport protein not involved directly in acid secretion, also was evaluated. Results. Administration of pentagastrin caused dose-dependent increases in levels of mRNAs encoding H/K and BSC but had no significant effect on levels of Na/K mRNA. Administration of GRA prevented the pentagastrin-induced changes in mRNA levels for these transporters. Conclusions. Pentagastrin administration selectively up-regulates levels of mRNA encoding membrane proteins involved in acid secretion. The up-regulation of the mRNAs encoding BSC during pentagastrin stimulation indicates that regulation of basolateral Cl- movement may be as important as the regulation of apical H+ movement under stimulated states.",
author = "Klingensmith, {M. E.} and H. Hallonquist and McCoy, {B. P.} and Cima, {R. R.} and E. Delpire and Soybel, {D. I.}",
note = "Funding Information: GASTRIN FACIIJTATEST HE RELEASE of HCI from parietal cells via stimulation of histamine release from gastric enterochromaffinlike (ECL) cellsJ It is now recognized that histamine stimulates H,~ receptors located on the gastric parietal cell, resulting in luminal acid secretion. Gastrin receptors also have been exhibited on parietal cells, but most of the evidence indicates that these receptors play a small role in parietal cell acid secretion.l3 Instead, it is hypothesized that gastrin receptors on parietal cells mediate the well-recognized trophic effects of gastrin. 4-s Supported by National Institutes of Health awards F32 DK 09033 (M.K.), F32 DK 09288 (R.C.), and R29 DK 44571 (D.S.) and by a Davis and Geck research fellowshipo f the Associationf or Academic Surgery (M.K.). Presented at the Fifty-seventhA nnual Meeting of the Society of University Surgeons, Washington,D .C., Feb. 8-10, 1996. Reprint requests: David I. Soybel, MD, Division of General and GastrointestinalS urgery, Brigham and Women's Hospital, 75 Francis St., Boston, MA 02115. Copyright 9 1996 by Mosby-Year Book, Inc. 0039-6060/96/$5.00 + 0 11/6/73514 We hypothesized that in an in vivo rat model, exogenously administered pentagastrin would affect the levels of mRNAs encoding membrane proteins that are important in gastric acid secretion. The enzyme responsible for active transport of H + into the stomach lumen is H/K adenosine triphosphatase (H/K), found on the apical membrane of the gastric parietal cell. In many experimental situations the apical secretion ofH + by the parietal cells requires concomitant Ci-release, 9' l0 presumably through an apical C1-channel. 11 The secreted C1-is derived from the serosal solution that perfuses the basolateral surfaces of the fundic mucosa.10' 12, 13 Other researchers have established evidence for a C1-/HCO3-exchanger on the basolateral membrane of parietal cells, that serves as an entry site for cellular CI-J 4, 15 However, recent work in our laboratory provided evidence for an additional but unsuspected source for ba-solateral C1-uptake, a bumetanide-sensitive Na+-K+-C1-cotransporter (BSC). In an amphibian model we have shown that BSC may play a dominant role in the secretion of HC1 across the apical membrane during stimulated states of acid secretion. 1~ Therefore we sought to",
year = "1996",
doi = "10.1016/S0039-6060(96)80294-7",
language = "English (US)",
volume = "120",
pages = "242--247",
journal = "Surgery",
issn = "0039-6060",
publisher = "Mosby Inc.",
number = "2",
}