Distinctive effect of angiotensin II on prostaglandin production in dog renal and femoral arteries.
The effect of angiotensin II (Ang II) on prostaglandin (PG) production in dog renal and femoral vasculature was examined in vivo and in vitro. In pentobarbital anesthetized dogs, the reduction of blood flow induced by intra-arterial infusion of Ang II was potentiated by pre-treatment with indomethacin (5 mg/kg) in the renal but not the femoral vasculature. Isolated renal and femoral arterial strips were incubated and the release of PGE2 and PGI2 (as 6-keto-PGF1 alpha) into the medium was measured by radioimmunoassay. Basal PGE2 and PGI2 production by renal and femoral arterial strips was approximately the same. PGI2 production was predominant for both strips. Ang II stimulated PG production in renal but not femoral arteries. In the renal artery, Ang II-induced PG production was inhibited by indomethacin (10(-6) M), mepacrine (10(-4) M) and saralasin (10(-6) M). These results suggest that Ang II stimulates PG production by the renal artery per se and the Ang II receptor is linked to phospholipase A2 in the renal but not the femoral artery.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D015232:Dinoprostone; D004285:Dogs; D011464:Epoprostenol / Q000096:biosynthesis*; D005260:Female; D005263:Femoral Artery / Q000378:metabolism*; D005269:Femur / Q000098:blood supply; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply; D008297:Male; D011458:Prostaglandins E / Q000096:biosynthesis*; D011796:Quinacrine / Q000494:pharmacology; D012039:Regional Blood Flow / Q000187:drug effects; D012077:Renal Artery / Q000378:metabolism*; D012504:Saralasin / Q000494:pharmacology
D011458:Prostaglandins E; D000804:Angiotensin II; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D011796:Quinacrine; D012504:Saralasin; D015232:Dinoprostone; D007213:Indomethacin