Prostacyclin increases cAMP in coronary arteries.
This study was designed to determine whether prostacyclin (PGI2)-induced relaxation in circular strips of coronary arteries might be mediated by cAMP. Partially depolarized circular strips of bovine coronary arteries were used and PGI2-induced changes in length were compared with tissue concentrations of cAMP and cGMP, measured by RIA. It was found that PGI2 produced significant and concentration dependent increases in cAMP levels which were closely associated with the relaxant effects produced by the same concentrations (0.3 - 26.7 muM). Cyclic GMP was not changed by these concentrations. The relaxant effects of PGI2 were not antagonized by propranolol. There was a significant linear correlation between log increases in cAMP and percent relaxation produced by PGI2 which was almost identical with similar correlations obtained with either isoprenaline or adenosine, indicating that the relaxant effects of PGI2 are in analogy to those of isoprenaline and adenosine likely to be mediated by cAMP.
D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000187:drug effects; D002417:Cattle; D003331:Coronary Vessels / Q000187:drug effects*; D000242:Cyclic AMP / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000494:pharmacology*; D007545:Isoproterenol / Q000494:pharmacology; D009126:Muscle Relaxation; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D011433:Propranolol / Q000494:pharmacology; D011453:Prostaglandins / Q000494:pharmacology*
D011453:Prostaglandins; D011433:Propranolol; D011464:Epoprostenol; D000242:Cyclic AMP; D000241:Adenosine; D007545:Isoproterenol