Role of prostaglandin E2 in regulation of low and high water osmotic permeability in frog urinary bladder.

The water osmotic permeability of frog urinary bladder was found to be increased from 0.08 +/- 0.01 to 1.28 +/- 0.20 microl/min cm2 when serosal bathing medium was changed 4 times for a fresh Ringer solution. High epithelium permeability is accompanied by an increased content of cyclic AMP in the bladder tissue (by 42%, P < 0.01), higher activity of both basal and forskolin-stimulated membrane adenylate cyclase (AC) (by 109% and 74%, respectively, P < 0.05) and by appearance of aggregates of intramembranous particles in the apical membrane. The water flow was inhibited by 10(-9)-10(-5) M prostaglandin E2 (PGE2); the inhibitory effect was eliminated in the presence of 10(-4) M N-ethylmaleimide. The increase of water permeability due to changes of the bathing medium was accompanied by a decrease of serosal PGE2 concentration from 14.8 +/- 1.0 in the 1st solution to 0.6 +/- 0.1 nM in the 5th. 10(-6) M PGE2 in vitro inhibited the activity of membrane AC from highly permeable bladders by 33.4% (P < 0.02). Pretreatment of the membranes with 10 microg/ml pertussis toxin (PT) completely reversed this effect (+149%, P < 0.01). A significant activation of AC was also observed under 10(-10) M PGE2 (by 196%). These data demonstrate that the water permeability could be markedly increased independently of ADH, suggesting that the trigger role in activation of water transport is played by a decreased level of PGE2 which could stimulate AC.