Prostaglandin E2 and I2 production in isolated dog renal arteries in the absence or presence of vascular endothelial cells.
The spontaneous prostaglandin I2 production was significantly reduced by the removal of endothelial cells from the isolated dog renal arteries compared with relative slight reduction of prostaglandin E2 production. The stimulation of prostaglandin I2 production induced with angiotensin II was also markedly reduced under the absence of endothelial cells, while its potentiation of prostaglandin E2 production was not inhibited. The results suggest that the vascular endothelial cells are the major sources of prostaglandin I2 in the dog renal arteries, while prostaglandin E2 is mainly produced in other cell types, perhaps vascular smooth muscle cells.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D015232:Dinoprostone; D004285:Dogs; D004727:Endothelium / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D005260:Female; D007700:Kinetics; D008297:Male; D011458:Prostaglandins E / Q000096:biosynthesis*; D012077:Renal Artery / Q000187:drug effects / Q000378:metabolism*
D011458:Prostaglandins E; D000804:Angiotensin II; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D015232:Dinoprostone