Stimulation by Prostaglandin E2 of Alkaline Secretion in the Rat Duodenum: Comparative Study with Hypertonic NaCI
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- TAKEUCHI Koji
- Department of Applied Pharmacology, Kyoto Pharmaceutical University
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- NIIDA Hiromichi
- Department of Applied Pharmacology, Kyoto Pharmaceutical University
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- TAKINAMI Yusuke
- Department of Applied Pharmacology, Kyoto Pharmaceutical University
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- OKABE Susumu
- Department of Applied Pharmacology, Kyoto Pharmaceutical University
書誌事項
- タイトル別名
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- Stimulation by prostaglandin E2 of alkaline secretion in the rat duodenum: Comparative study with hypertonic NaCl.
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説明
Possible involvement of increased mucosal permeability in the stimulation by prostaglandin E2 (PGE2) of duodenal HCO3- secretion was investigated in rats. PGE2 (0.3, 1 mg/kg, s.c.) dose-dependently increased HCO3- secretion in the duodenum with a significant elevation of transmucosal potential difference (PD); the PD was increased from -4.5 ± 0.3 mV to -10.0 ± 1.5 mV (mucosa negative) at 1 mg/kg. These responses caused by PGE2 were abolished by sacrificing the animals with saturated KCl (i.v.). Although a significant increase of HC03-output was observed after exposure of the mucosa to 1 M NaCl (0.5 ml), this response was accompanied by a significant reduction of PD and was not abolished after KCl injection. The mucosal permeability determined by Evans blue (1%, i.v.) was not affected by PGE2, while 1 M NaCl markedly elevated the amount of extravasated dye in both the luminal content and the mucosa. Stimulation of HC03-output by PGE2 was significantly mitigated by ouabain (3 mg/kg, s.c.) or prior exposure of the mucosa to 1 M NaCl. These results suggest that stimulation by PGE2 of duodenal HCO3- secretion is not simply due to the increased mucosal permeability, but depends rather on both the Na/K ATPase activity and the intact perfusion of the organ. The HCO3- response as induced by 1 M NaCl may result from the increased permeability and is accompanied by a marked reduction of PD.
収録刊行物
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- Jpn.J.Pharmacol.
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Jpn.J.Pharmacol. 53 (1), 67-74, 1990
公益社団法人 日本薬理学会
