Article
Helicobacter pylori augments the acid
inhibitory effect of omeprazole on parietal cells and gastric
H+/K+-ATPase
W Beila, K-F Sewinga, R Buschec, S Wagnerb
a Department of
General Pharmacology, Hannover Medical School, Hannover, Germany, b Department of
Gastroenterology and Hepatology, Hannover Medical School, Hannover,
Germany, c Department of
Physiology, School of Veterinary Medicine, Hannover, Germany
Correspondence to: Dr W Beil, Department of
General Pharmacology, Medizinische Hochschule Hannover,
Carl-Neuberg-Stra
e 1, D-30625 Hannover, Germany.
Beil.Winfried@MH- Hannover.de
Accepted for publication 8 August 2000
BACKGROUND
In duodenal
ulcer patients, intragastric acidity during omeprazole treatment is
significantly lower before Helicobacter
pylori eradication than after cure.
AIMS
To determine if
H pylori enhances the acid inhibitory
potency of omeprazole in isolated parietal cells and on
H+/K+-ATPase.
METHODS
Rat parietal
cells and pig gastric membrane vesicles enriched in
H+/K+-ATPase activity were incubated with
H pylori and the H
pylori fatty acid cis
9,10-methyleneoctadecanoic acid (MOA), and the inhibitory effects of
omeprazole on parietal cell acid production, H+/K+-ATPase enzyme activity, and ATPase
mediated proton transport were assessed.
RESULTS
In isolated
parietal cells, H pylori and MOA increased
the acid inhibitory potency of omeprazole 1.8 fold.
H pylori did not affect the inhibitory
potency of omeprazole on H+/K+-ATPase enzyme
activity. In proton transport studies, H
pylori (intact bacteria and sonicate) and MOA accelerated the
onset of the inhibitory effect of omeprazole and enhanced the proton
dissipation rate in response to omeprazole. H
pylori itself increased proton permeability at the vesicle membrane.
CONCLUSION
Our results
show that H pylori augments the acid
inhibitory potency of omeprazole in parietal cells and enhances
omeprazole induced proton efflux rate from gastric membrane vesicles.
We suggest that omeprazole unmasks the permanent effect of
H pylori on proton permeability at the
apical parietal cell membrane, which is counteracted in the absence of
a proton pump inhibitor by a reserve
H+/K+-ATPase capacity.
Keywords: H pylori; parietal cells; omeprazole; H+/K+-ATPase
© 2001 by Gut
This article has been cited by other articles:
-
Sgouros, S N, Bergele, C
(2006). Clinical outcome of patients with Helicobacter pylori infection: the bug, the host, or the environment?. Postgrad. Med. J.
82: 338-342
[Abstract] [Full Text]
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