Role of prostaglandin in the regulation of gastric H(+)-Transporting system

Prostaglandins and (PG) have been reported to be an important gastric acid suppressive factor. However, the mechanism underlying is yet to be clearly established. In vitro study with gastric microsomes in presence of both PGE(2) and PGI(2) shows a stimulation of gastric H(+) K(+)-ATPase activity below 1X10(-6)M and 2.5X10(-7)M concentrations respectively. However, with further increase in concentrations of both PGE(2) and PGI(2), H(+), K(+)-ATPase activity shows an inhibition but PGI(2) completely obliterates the K(+) stimulated part of H(+), K(+)-ATPase activity at higher concentration. The H(+)-ion transport study using chambered frog gastric mucosa shows that both PGE(2) and PGI(2) inhibit H(+)-ion transport at 5X10(-6) M and 10X10(-6)M concentrations respectively but the effect of PGI(2) is reversible. These differential effects of PGE(2) and PGI(2) on microsomal H(+), K(+)-ATPase and on H(+) transport my be caused by the differential effects of these phospholipid mediators with the gastric mucosal cell membrane. This in vitro investigation shows the role of prostaglandin (s) as a physiological switch/regulator of gastric H(+) ion transport leading to the cessation of gastric acid secretion.