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1
Content available Does the membrane potential control incorporation of tubulovesicles into the secreting apical membrane of the rat parietal cell?
100%
Ostrowski J. , Dolowy K. , Zych W. , Butruk E.
Journal of Physiology and Pharmacology
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1991
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tom 42
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nr 4
EN
The present studies were designed to examine the effect of changes in membrane potential by means of protonophore carbonyl cyanide m-chlorophenylhydrazone (СССР) and variations in the pH of the medium on the secretory response of parietal cells. Studies were performed in vitro using isolated cells from rat stomachs and acid production was indirectly determined by ¹⁴C-aminopyrine (AP) accumulation. СССР affected both basal and histamine-stimulated AP accumulation in a concentration-dependent manner. The AP accumulation ratios depended on pH of the incubation medium; the ratio was lowest at pH 6.6, and increased progressively as the pH of the medium increased to 7.8. Moreover, the decreases in AP accumulation ratios caused by simultanous addition of СССР and AP to cell suspensions compared to those in which СССР was added to incubated cells after achieving the steady-state of AP accumulation were quantitatively similar. These findings suggest that the decrease in AP accumulation due to СССР treaiment is a consequence of an activation of acid secretion rather than an inhibitor of acid production. From the present and previously published data, we propose a working hypothesis: membrane recycling is dependent on changes in apical membrane potential.
2
Content available remote Pharmacological regulation of gastric acid secretion in the apical membrane of parietal cells; a new target for antisecretory drugs
100%
Okabe S. , Shimosako K. , Amagase K.
Journal of Physiology and Pharmacology
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2001
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tom 52
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nr 4,1
EN
We examined the local effect of several drugs against secretagogue-stimulated acid secretion in dogs. Test drugs were applied to denervated gastric pouches in conscious dogs either for 5 to 30 min beginning 1 hr after or for 30 min before intravenous infusion of gastric secretagogues (histamine, pentagastrin, or carbachol). The antisecretory effect of test drugs delivered by an intravenous or oral route was also examined. Local application of acid pump inhibitors (omeprazole, leminoprazole) for 30 min beginning l hr after histamine infusion significantly inhibited gastric acid secretion. The effect of leminoprazole persisted for more than 8 hr after a 30 min application. A mast cell stabilizer (FPL 52694) applied to pouches for 15 to 30 min also potently inhibited histamine-stimulated gastric acid secretion in a time-dependent manner. The duration of the antisecretory effect of such drugs after a 30 min application was greater than 4 hr. Locally applied leminoprazole and FPL 52694 for 30 min also significantly inhibited pentagastrin- and carbachol-stimulated gastric acid secretion. Although intravenous omeprazole and leminoprazole exerted a potent antisecretory effect on histamine-induced acid secretion FPL 52694 had little or no antisecretory effect following intravenous or oral administration. 16, 16-dimethyl prostagladin E2 also locally inhibited histamine-stimulated acid secretion. Acid stable local anesthetics (tetracaine, ethyl-4-aminobenzoate), histamine H2-receptor blockers (cimetidine, ranitidine, and famotidine), and a muscarinic M1-receptor antagonist (pirenzepine) did not exhibit local antisecretory effects. Such results strongly suggest that the apical membrane of parietal cells possesses a pharmacologically sensitive portion similar to the basolateral membrane, which usually mediates gastric acid secretion. The apical membrane represents an intriguing target for new antisecretory drugs, as well as a new medium for further elucidating the functional features of parietal cells.
3
Content available The relationship between extracellular K-plus and Ca2-plus on aminopyrine accumulation in rat parietal cells
86%
Ostrowski J. , Zych W. , Dolowy K. , Butruk E.
Journal of Physiology and Pharmacology
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1991
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tom 42
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nr 3
EN
The effects of extracellular K⁺ in relation to extracellular Ca²⁺ on acid production were studied. Studies were performed in vitro using isolated cells from rat stomachs, and acid production was indirectly determined by ¹⁴C-aminopyrine (AP) accumulation. In the absence of K⁺ in the incubation medium histamine-stimulated AP accumulation ratios were significantly decreased independently in the presence or absence of extracellular Ca²⁺. Under basal conditions, in the absence of extracellular Ca²⁺ , increasing concentrations of extracellular K⁺ enhanced AP accumulation ratios to significantly higher than those found in the presence of Ca²⁺. In histamine-, cAMP-, and carbachol-stimulated parietal cells, high K⁺ concentrations increased AP accumulation significantly less in Ca²⁺-free than in Ca²⁺-containing media. High K⁺ also induced significantly both an increase in cytosolic free Ca²⁺ concentration and ⁴⁵ Ca²⁺ uptake. The present results confirmed the importance of K⁺ in gastric acid production and suggested a role for Ca²⁺ as a modulator of mechanisms of parietal cell stimulation.
4
Content available Functional and structural changes of isolated rat parietal cells during membrane potential modulation
72%
Ostrowski J. , Jarosz D. , Zych W. , Wojciechowski K.
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|
nr 3
5
Content available remote Phosphodiesterase isozymes involved in regulating acid secretion in the isolated mouse stomach
58%
Okuda S. , Honda M. , Ito Y. , Aihara E. , Kato S. , Mitsufuji S. , Yoshikawa T. , Takeuchi K.
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tom 60
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nr 7
6
Content available Effects of acid-degraded products of leminoprazole on acid secretion, mucus secretion and synthesis and indomethacin-induced damage in cell culture
58%
Takahashi S. , Tsukahara T. , Okabe S.
Journal of Physiology and Pharmacology
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1998
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tom 49
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nr 1
7
Evidence for impaired gastric acid secretion in H.pylori gastritis with antigastric autoantibodies
58%
Faller G. , Winter M. , Konturek S. J. , Konturek P. C. , Kirchner T.
Journal of Physiology and Pharmacology. Supplement
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1997
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tom 48
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nr 1
8
Content available The role of H. pylori infection in the pathophysiology of duodenal ulcer disease
51%
McColl K. E. L. , El-Omar E. M. , Gillen D.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 3
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