scholarly journals Inhibitory Effect of Leminoprazole on Acid Secretion in Parietal Cells Isolated from Guinea Pig Gastric Mucosa

1995 ◽  
Vol 68 (1) ◽  
pp. 19-23 ◽  
Author(s):  
Eiichi Saito ◽  
Yutaka Matsuo
Keyword(s):  
Gastric Mucosa ◽  
Guinea Pig ◽  
Acid Secretion ◽  
Inhibitory Effect ◽  
Parietal Cells

Succinic and Malic Oxidase in Gastric Hydrochloric Acid Production

1956 ◽  
Vol 187 (3) ◽  
pp. 427-431 ◽  
Author(s):  
Joseph J. Vitale ◽  
Oscar M. Jankelson ◽  
Patricia Connors ◽  
D. Mark Hegsted ◽  
Norman Zamcheck
Keyword(s):  
Gastric Mucosa ◽  
Guinea Pig ◽  
Succinic Dehydrogenase ◽  
Titratable Acidity ◽  
Spectrophotometric Analysis ◽  
Parietal Cells ◽  
Human Gastric Mucosa ◽  
City Hospital ◽  
Malic Dehydrogenase ◽  
Oxidase System

Effect of histamine on the activity of succinic oxidase and malic dehydrogenase was studied in guinea pig and human gastric mucosa. Human tissue was obtained through the surgical services of the Boston City Hospital. Control value for the succinic oxidase system of the proximal half of the guinea pig stomach was approximately 480 ( Qo2 (N) (µl O2/mg nitrogen/hr.)). After histamine, this value rose to 550 in 30 minutes with a simultaneous rise in titratable acidity of the stomach contents. Animals fasted for 72 hours had a Qo2 (N) of approximately 500 and after histamine a Qo2 (N) of 700 was observed. Spectrophotometric analysis of succinic dehydrogenase and cytochrome oxidase activities, two of the major components of the succinic oxidase system, revealed that both components are increased following histamine administration. Malic dehydrogenase, however, was not affected by histamine treatment. Succinic dehydrogenase was demonstrated by histochemical localization and was concentrated below the superficial mucous layer where parietal cells were abundant. Succinic oxidase activity of human gastric mucosa was demonstrable only in those specimens containing abundant parietal cells. This study confirms the view that HCl production by parietal cells is associated with aerobic metabolism and is perhaps under enzymatic control. The study suggests that the succinic oxidase system may be involved in the production or secretion of HCl.

Stereospecific Inhibition by Naloxone of Histamine-Stimulated Acid Secretion in Isolated Guinea Pig Parietal Cells

Pharmacology ◽  
1984 ◽  
Vol 29 (6) ◽  
pp. 320-328 ◽  
Author(s):  
W. Kromer ◽  
P. Schröder ◽  
S. Netz
Keyword(s):  
Guinea Pig ◽  
Acid Secretion ◽  
Parietal Cells

Regulation of acid secretion by bombesin/GRP neurons of the gastric fundus

1991 ◽  
Vol 260 (1) ◽  
pp. G156-G160 ◽  
Author(s):  
M. L. Schubert ◽  
J. Hightower ◽  
D. H. Coy ◽  
G. M. Makhlouf
Keyword(s):  
Acid Secretion ◽  
Cholinergic Neurons ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Gastric Fundus ◽  
Parietal Cells ◽  
Inhibitory Influence ◽  
Field Stimulation ◽  
Somatostatin Secretion ◽  
Direct Inhibitory Effect

Intramural neurons in the fundus of the isolated mouse stomach were activated by 1,1-dimethyl-4-phenylpiperazinium (DMPP) or by electrical field stimulation and the participation of cholinergic and bombesin/gastrin-releasing peptide (GRP) neurons in the regulation of acid secretion evaluated with atropine and a selective bombesin/GRP antagonist, [Leu13-psi(CH2NH)-Leu14]bombesin. For both DMPP and field stimulation, atropine inhibited acid secretion and augmented somatostatin secretion. The bombesin/GRP antagonist had an opposite effect, augmenting acid secretion and inhibiting somatostatin secretion to below basal levels. The combination of the two antagonists restored DMPP- and field-stimulated acid and somatostatin secretion to basal levels. The results indicate that neurally stimulated acid secretion in the isolated mouse stomach is regulated by cholinergic neurons that mediate stimulation and bombesin/GRP neurons that mediate inhibition of acid secretion. Cholinergic neurons exert their stimulatory effect by acting directly on parietal cells and indirectly by eliminating the inhibitory influence of somatostatin. Bombesin/GRP neurons exert their inhibitory effect mainly by inducing release of somatostatin; an additional direct inhibitory effect of bombesin/GRP neurons on parietal cells is possible.

scholarly journals Immunocytochemical identification of low-affinity NTS2 neurotensin receptors in parietal cells of human gastric mucosa

2006 ◽  
Vol 191 (1) ◽  
pp. 121-128 ◽  
Author(s):  
Stefan Schulz ◽  
Christoph Röcken ◽  
Matthias P A Ebert ◽  
Solveig Schulz
Keyword(s):  
Plasma Membrane ◽  
Gastric Mucosa ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Parietal Cells ◽  
Neuroendocrine Cells ◽  
Target Cells ◽  
Human Gastric Mucosa ◽  
Western Blots

The biological effects of neurotensin (NT) are mediated by two distinct G protein-coupled receptors, NTS1 and NTS2. Although it is well established that neurotensin inhibits gastric acid secretion in man, the plasma membrane receptor mediating these effects has not been visualized yet. We developed and characterized a novel antipeptide antibody to the carboxy-terminal region of the human NTS2 receptor. The cellular and subcellular distribution of NTS2 receptors was evaluated in various human gastrointestinal tissues. Specificity of the antiserum was demonstrated by (1) detection of a broadband migrating at Mr 90 000–100 000 in Western blots of membranes from NTS2-expressing tissues; (2) cell-surface staining of NTS2-transfected cells; (3) translocation of NTS2 receptor immunostaining after agonist exposure; and (4) abolition of tissue immunostaining by preadsorbtion of the antibody with its immunizing peptide. In the gastrointestinal tract, NTS2 receptor immunoreactivity was highly abundant in parietal cells of the gastric mucosa, in neuroendocrine cells of the stomach small and large intestine, and in cells of the exocrine pancreas. NTS2 receptors were clearly located in the plasma membrane and uniformly present on nearly all target cells. The presence of NTS2 receptors was rarely detected in human tumors. This is the first localization of NTS2 receptors in human formalin-fixed, paraffin-embedded tissues at the cellular level. The abundant expression of low-affinity NTS2 receptors on the plasma membrane of human parietal cells provides a morphological substrate for the direct inhibition of gastric acid secretion observed after i.v. administration of neurotensin.

scholarly journals Isolation of parietal cells from guinea-pig gastric mucosa and the immunological characterization of their antigenic structure.

Gut ◽  
1975 ◽  
Vol 16 (8) ◽  
pp. 603-612 ◽  
Author(s):  
D P Jewell ◽  
V N Katiyar ◽  
C Rees ◽  
K B Taylor ◽  
J P Wright
Keyword(s):  
Gastric Mucosa ◽  
Guinea Pig ◽  
Parietal Cells ◽  
Antigenic Structure ◽  
Immunological Characterization

scholarly journals Acid secretion-associated translocation of KCNJ15 in gastric parietal cells

2011 ◽  
Vol 301 (4) ◽  
pp. G591-G600 ◽  
Author(s):  
Wenjun He ◽  
Wensheng Liu ◽  
Catherine S. Chew ◽  
Susan S. Baker ◽  
Robert D. Baker ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Western Blot ◽  
Acid Secretion ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Apical Membrane ◽  
Parietal Cells ◽  
Immunofluorescence Staining ◽  
Gastric Glands ◽  
Gastric Parietal Cells

Potassium ions are required for gastric acid secretion. Several potassium channels have been implicated in providing K+ at the apical membrane of parietal cells. In examining the mRNA expression levels between gastric mucosa and liver tissue, KCNJ15 stood out as the most highly specific K+ channel in the gastric mucosa. Western blot analysis confirmed that KCNJ15 is abundant in the stomach. Immunofluorescence staining of isolated gastric glands indicated that KCNJ15 was expressed in parietal cells and chief cells, but not in mucous neck cells. In resting parietal cells, KCNJ15 was mainly found in puncta throughout the cytoplasm but was distinct from H+-K+-ATPase. Upon stimulation, KCNJ15 and H+-K+-ATPase become colocalized on the apical membranes, as suggested by immunofluorescence staining. Western blot analysis of the resting and the stimulated membrane fractions confirmed this observation. From nonsecreting preparations, KCNJ15-containing vesicles sedimented after a 4-h centrifugation at 100,000 g, but not after a 30-min spin, which did sediment most of the H+-K+-ATPase-containing tubulovesicles. Most of the KCNJ15 containing small vesicle population was depleted upon stimulation of parietal cells, as indicated by the fact that the KCNJ15 signal was shifted to a large membrane fraction that sedimented at 4,000 g. Our results demonstrate that, in nonsecreting parietal cells, KCNJ15 is stored in vesicles distinct from the H+-K+-ATPase-enriched tubulovesicles. Furthermore, upon stimulation, KCNJ15 and H+-K+-ATPase both translocate to the apical membrane for active acid secretion. Thus KCNJ15 can be added to the family of apical K+ channels in gastric parietal cells.

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