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The relationship between extracellular K-plus and Ca2-plus on aminopyrine accumulation in rat parietal cells

100%

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

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.

2

Roles of endogenous prostaglandins and cyclooxygenase isozymes in mucosal defense of inflamed rat stomach

84%

Takeeda M., Hayashi Y., Yamato M., Murakami M., Takeuchi K.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,2

Endogenous prostaglandins (PGs) are involved in adaptive gastric protection against acute injury, and cyclooxygenase (COX)-1 is responsible for the production of PGs in this phenomenon. In the present study, we examined the effect of various COX inhibitors on gastric ulcerogenic and acid secretory responses following daily exposure of the stomach to iodoacetamide (IA) and investigated the role for COX isozyme in gastric protection under subchronic mucosal irritation. Gastric mucosal irritation was induced by addition of 0.1% IA to drinking water, and the gastric mucosa was examined on the 6th day. Indomethacin (5 mg/kg) or SC-560 (selective COX-1 inhibitor, 5 mg/kg) or rofecoxib (selective COX-2 inhibitor, 5 mg/kg) was given p.o. twice 24 hr and 3 hr before the termination of IA treatment. Giving IA in drinking water for 5 days produced minimal damage in the stomach. The damage was significantly worsened by indomethacin, resulting in hemorrhagic lesions. Both SC-560 and rofecoxib also aggravated such lesions, although the effect of rofecoxib was more pronounced. Treatment with IA decreased acid secretion in pylorus-ligated stomachs, and this change was significantly reverted by indomethacin as well as SC-560 and rofecoxib. Mucosal PGE2 content was increased following IA treatment, with apparent expression of COX-2 mRNA in the stomach, and the increased PGE2 production was significantly suppressed by SC-560 and rofecoxib as well as indomethacin. These results suggest that endogenous PGs derived from both COX-1 and COX-2 are involved in the mucosal defense of the inflamed stomach, partly by decreasing acid secretion and contribute to maintaining the mucosal integrity under such conditions.

3

A new model of gastric bleeding induced in rats by aspirin plus clopidogrel under stimulation of acid secretion. Prophylactic effects of antiulcer drugs

67%

Takayama S., Izuhara C., Yamada N., Yamanaka S., Hashimoto E., Kaneko S., Takeuchi K.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 1

4

Eradication of Helicobacter pylori and gastrin-somatostatin link in duodenal ulcer patients

67%

Konturek J. W., Bielanski W., Konturek S. J., Domschke W.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 1

5

Stimulation by nitric oxide of gastric acid secretion in bullfrog fundic mucosa in vitro

67%

Kawauchi S., Sugamoto S., Furukawa O., Mimaki H., Takeuchi K.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 1

6

Involvement of prostaglandin E receptor EP3 subtype and prostacyclin IP receptor in decreased acid response in damaged stomach

67%

Nishio H., Terashima S., Nakashima M., Aihara E., Takeuchi K.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 3

We investigated the roles of cyclooxygenase (COX) isozymes and prostaglandin E (PGE) receptor EP1 and EP3 subtypes or prostacyclin IP receptors in the decrease in acid secretion in the damaged mouse stomach. Male C57/BL6 mice, both wild type and animals lacking EP1, EP3, or IP receptors, were used after 18 h of fasting. Under urethane anesthesia, the stomach was mounted on an ex-vivo chamber and perfused with saline, and acid secretion as well as transmucosal potential difference (PD) was measured before and after exposure to 20 mM taurocholate Na (TC) for 20 min. Indomethacin, SC-560 or rofecoxib was given i.d. 30 min before TC. Mucosal exposure to TC in wild-type mice caused a reduction in PD, followed by decrease in acid secretion. Indomethacin attenuated the decrease in acid secretion after exposure to TC in wild-type mice, an effect mimicked by SC-560 but not rofecoxib, yet none of these drugs affected the decrease in PD. An altered acid response after exposure to TC was similarly observed in EP1 (-/-) mice but mitigated in mice lacking either EP3 or IP receptors, although a decrease in PD was observed in all groups. Furthermore, the decreased acid response was also attenuated by prior administration of the EP3- but not EP1- antagonist. Mucosal levels of PGE2 and 6-keto PGF1alpha increased after exposure to TC in all groups of mice. In conclusion, the decrease in acid secretion in the damaged stomach is mediated by endogenous PGs derived from COX-1, through PGE2/EP3 receptors and prostacyclin/IP receptors.

7

H.pylori corpus gastritis - relation to acid output

67%

Sipponen P., Hyvarinen H., Siurala M.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 1

8

Effects of acid-degraded products of leminoprazole on acid secretion, mucus secretion and synthesis and indomethacin-induced damage in cell culture

67%

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

9

Strategies for Helicobacter pylori eradication in 1995: A review of international and Belgian experience

67%

Deltenre M., Jonas C., Otero J., Cozzoli A., Denis P., Burette A., De Koster E.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 1

Ograniczanie wyników

The relationship between extracellular K-plus and Ca2-plus on aminopyrine accumulation in rat parietal cells

Roles of endogenous prostaglandins and cyclooxygenase isozymes in mucosal defense of inflamed rat stomach

A new model of gastric bleeding induced in rats by aspirin plus clopidogrel under stimulation of acid secretion. Prophylactic effects of antiulcer drugs

Eradication of Helicobacter pylori and gastrin-somatostatin link in duodenal ulcer patients

Stimulation by nitric oxide of gastric acid secretion in bullfrog fundic mucosa in vitro

Involvement of prostaglandin E receptor EP3 subtype and prostacyclin IP receptor in decreased acid response in damaged stomach

H.pylori corpus gastritis - relation to acid output

Effects of acid-degraded products of leminoprazole on acid secretion, mucus secretion and synthesis and indomethacin-induced damage in cell culture

Strategies for Helicobacter pylori eradication in 1995: A review of international and Belgian experience