ACTION OF PROSTAGLANDIN DEHYDROGENASE INHIBITORS ON PROSTAGLANDIN UPTAKE IN RAT ISOLATED LUNG

The effects of some inhibitors of 15‐hydroxy‐prostaglandin dehydrogenase (PGDH) have been studied on the inactivation of prostaglandin E2 (PGE2) and 16, 16‐dimethyl PGE2 in rat isolated lung. Bioassay was used to show that the inactivation of PGE2 and its methyl analogue, was inhibited by frusemide (10−3m), N‐ethyl maleimide (10−5m) and 5, 5′‐dithio‐bis‐2‐nitro‐benzoic acid (10−2m), but not by caffeine (2.5 × 10−3m). The efflux of radioactivity from lung following injection of [14C]‐PGE2 was faster in lungs treated with frusemide, N‐ethyl maleimide or bromcresol green, than in untreated lungs. Caffeine (10−3, 10−2m) did not change the rate of 14C‐efflux from lungs following injection of [14C]‐PGE2. From these results it is concluded that those PGDH inhibitors that prevented prostaglandin inactivation in isolated lungs did so by inhibiting uptake of prostaglandin rather than by inhibiting PGDH. 1979 British Pharmacological Society