Coronary vasodilation: interactions between prostacyclin and adenosine.
1 The influence of prostacyclin (PGI2) on the release of adenosine in rabbit hearts perfused by the Langendorff method was examined under normal conditions of perfusion and during perfusion with the adenosine antagonist, aminophylline. 2 PGI2 increased both coronary flow and the myocardial release of adenosine in a dose-dependent manner. Aminophylline at a low concentration (10 microgram/ml) suppressed the enhanced flow. 3 Adenosine increased both coronary flow and the release of PGI2 from the isolated hearts; both these effects were inhibited by the low aminophylline concentration. Inhibition of PGI2-biosynthesis by 75% caused only a nonsignificant reduction in the adenosine-induced enhancement of coronary flow. 4 Aminophylline at a high concentration (50 microgram/ml) produced an increase in coronary flow and in release of PGI2 as did adenosine; neither of these effects was observed with the low concentration of aminophylline (10 microgram/ml). 5 It is suggested that the coronary vasodilator effects of PGI2 in the isolated perfused rabbit hearts are due, at least partially, to the release of adenosine.
D000241:Adenosine / Q000494:pharmacology*; D000628:Aminophylline / Q000494:pharmacology; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects*; D004347:Drug Interactions; D011464:Epoprostenol / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects; D011453:Prostaglandins / Q000494:pharmacology*; D011817:Rabbits; D014664:Vasodilation / Q000187:drug effects*
D011453:Prostaglandins; D000628:Aminophylline; D011464:Epoprostenol; D000241:Adenosine