Pulmonary uptake of PGE2 is inhibited by dipyridamole in rat isolated lungs.
The metabolism of prostaglandin E2 (PGE2) is decreased by dipyridamole (20 microM) in rat isolated perfused lungs. The inhibition of the metabolism is reversible as the decreased metabolism returned to the control level when pulmonary infusion of dipyridamole was abolished. After pulmonary injection of 14C-PGE2 (10 nmol) the radioactivity appeared more rapidly in the effluent when dipyridamole was infused into pulmonary circulation. Dipyridamole in vitro did not change the activity of 15-hydroxyprostaglandin dehydrogenase (15-OH-PGDH) in the 100,000 x g supernatant fraction of homogenized lungs. Thus, the decreased metabolism seems to be due to the inhibition of the uptake of PGE2 into the lungs. When the rats were pretreated with dipyridamole in drinking water for one week the activity of 15-OH-PGDH in the 100,000 x g supernatant fraction of the lungs was not changed significantly.
D000818:Animals; D015232:Dinoprostone; D004176:Dipyridamole / Q000494:pharmacology*; D006911:Hydroxyprostaglandin Dehydrogenases / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D011458:Prostaglandins E / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D011458:Prostaglandins E; D004176:Dipyridamole; D006911:Hydroxyprostaglandin Dehydrogenases; D015232:Dinoprostone