Stimulation by Prostaglandin E_2 of Alkaline Secretion in the Rat Duodenum

• Published in: Japanese Journal of Pharmacology 1990, Vol.53 (1), p.67-74
• Main Authors: Koji TAKEUCHI, Hiromichi NIIDA, Yusuke TAKINAMI, Susumu OKABE
• Format: Article
• Language: Japanese
• ISSN: 0021-5198

Possible involvement of increased mucosal permeability in the stimulation by prostaglandin E_2 (PGE_2 ) of duodenal HCO_3 ^- secretion was investigated in rats. PGE_2 (0.3, 1 mg/kg. s.c.) dose-dependently increased HCO_3 ^- 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 PGE_2 were abolished by sacrificing the animals with saturated KCI (i.v.). Although a significant increase of HCO_3 ^- output was observed after exposure of the mucosa to 1 M NaCI (0.5 ml), this response was accompanied by a significant reduction of PD and was not abolished after KCI injection. The mucosal permeability determined by Evans blue (1%, i.v.) was not affected by PGE_2 , while 1 M NaCI markedly elevated the amount of extravasated dye in both the luminal content and the mucosa. Stimulation of H COj output by PGE_2 was significantly mitigated by ouabain (3 mg/kg, s.c.) or prior exposure of the mucosa to 1 M NaCI. These results suggest that stimulation by PGE_2 of duodenal HCO_3 ^- 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 HCO_3 ^- response as induced by 1 M NaCI may result from the increased permeability and is accompanied by a marked reduction of PD.