Adenosine metabolism in cultured chick-embryo heart cells.

Adenosine, a coronary vasodilator, in involved in the regulation of coronary blood flow, but the mechanism (s) of vasodilation especially with respect to the influence of dipyridamole and aminophylline are not clearly understood. Cultured cardiac cells of 16-day-old chick embryos were used as a model for the mammalian heart. Hypoxia produced a twofold increase in the production of adenosine and its metabolic products in this preparation, indicating that the source of adenosine in the hypoxic heart is the myocardial cell. Neither dipyridamole (1 times 10-minus 6M) nor aminophylline (1 times 10-minus 5M) blocked the release of adenosine from the myocardial cells, but dipyridamole aminophylline was without effect. These data suggest that dipyridamole exerts its vasodilator effect by blocking the uptake of adenosine into the cells, thereby increasing its extracellular levels and the concentration of adenosine in the vicinity of coronary resistance vessels. The mechanism whereby aminophylline attenuates the vasodilation produced by adenosine is not known. However, aminophylline does not interfere with the release or uptake of adenosine.