We have previously demonstrated that neonatal rat stomach is less susceptible to luminal H+ when compared with the adult. In the present study we investigate the role of endogenous prostaglandins (PG) in the ontogeny of gastric permeability responses to H+. Responses to luminal instillation of 250 mN HCl were measured in rats at 10, 15, 20, and 25 days after birth. Mucosal responses were measured in terms of loss of H+ and appearance of Na+, K+, and protein in the luminal instillate. Indomethacin (IM; 8 mg/kg sc) administration to rat pups reduced mucosal levels of prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha). In response to intraluminal HCl, the reduction of mucosal PG did not significantly affect transmucosal fluxes of ions and protein when compared with control pups. IM was also given to lactating dams on days just prior to the pups being 10, 15, 20, and 25 days old. IM treatment significantly reduced the content of PGE2 and 6-keto-PGF1 alpha in maternal milk. Permeability responses in pups from IM-treated dams were increased over pups from control dams. This effect was not observed in 25-day-old rats. Treatment of pups from IM-injected dams with PGE2 but not PGI2 partially restored the permeability responses to luminal H+ to levels observed in pups from control dams.(ABSTRACT TRUNCATED AT 250 WORDS)
Role of bradykinin in the hyperaemia following acid challenge of the rat gastric mucosa