Stimulation by prostaglandin E2 of alkaline secretion in the rat duodenum: Comparative study with hypertonic NaCl.

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  • TAKEUCHI Koji
    Department of Applied Pharmacology, Kyoto Pharmaceutical University
  • NIIDA Hiromichi
    Department of Applied Pharmacology, Kyoto Pharmaceutical University
  • TAKINAMI Yusuke
    Department of Applied Pharmacology, Kyoto Pharmaceutical University
  • OKABE Susumu
    Department of Applied Pharmacology, Kyoto Pharmaceutical University

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  • Stimulation by Prostaglandin E2 of Alkaline Secretion in the Rat Duodenum: Comparative Study with Hypertonic NaCI

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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.

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