Effects of calcium antagonists and calmodulin inhibitors on angiotensin II-induced prostaglandin productions in the isolated dog renal arteries.
Angiotensin II markedly potentiated both PGE2 and PGI2 productions in the isolated dog renal arteries. This angiotensin II-induced response was significantly reduced by the treatments of EGTA and calcium antagonists such as verapamil, nifedipine and 8-(N,N'-diethylamino)-octyl-3,4,5,-trimethoxybenzoate (TMB-8). Calmodulin inhibitors, trifluoperazine and W-7 also inhibited the angiotensin II-induced PG productions while an inactive analogue of W-7, W-5 did not have any effect. The results suggest that angiotensin II may enhance the intracellular Ca2+ level through the influx of extracellular Ca2+ and then, calmodulin activated with Ca2+ will stimulate both PGE2 and PGI2 productions via its activation of phospholipase A2 in the dog renal arteries.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002147:Calmodulin / Q000037:antagonists & inhibitors*; D015232:Dinoprostone; D004285:Dogs; D004533:Egtazic Acid / Q000494:pharmacology; D005260:Female; D005707:Gallic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D008297:Male; D009543:Nifedipine / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis*; D011458:Prostaglandins E / Q000096:biosynthesis; D012077:Renal Artery / Q000187:drug effects / Q000378:metabolism*; D013449:Sulfonamides / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
D002121:Calcium Channel Blockers; D002147:Calmodulin; D011453:Prostaglandins; D011458:Prostaglandins E; D013449:Sulfonamides; D000804:Angiotensin II; D004533:Egtazic Acid; C006014:8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate; D015121:6-Ketoprostaglandin F1 alpha; D005707:Gallic Acid; C017967:W 7; C034700:N-(6-aminohexyl)-1-naphthalenesulfonamide; D014700:Verapamil; D009543:Nifedipine; D015232:Dinoprostone