STIMULATION BY PROSTAGLANDIN-E2 OF ALKALINE SECRETION IN THE RAT DUODENUM - COMPARATIVE-STUDY WITH HYPERTONIC NACL

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 KCI (i.v.). Although a significant increase of HCO3– 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 PGE2, while 1 M NaCI markedly elevated the amount of extravasated dye in both the luminal content and the mucosa. Stimulation of HCO3– output by PGE2 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 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 NaCI may result from the increased permeability and is accompanied by a marked reduction of PD. © 1990, The Japanese Pharmacological Society. All rights reserved.