Exogenous prostaglandin (PGE2) contracts bovine and human coronary arteries but its precursor, arachidonic acid, relaxes them. The endoperoxides PGH2 and PGH3 relax bovine coronary strips, but PGH1 produces contraction. The primary prostaglandins exert opposite effects to their own endoperoxide precursors, thus, PGE2 and PGE3 contract, and PGE1 relaxes the bovine coronary arteries. The paradoxical coronary dilation produced by the arachidonate or the PGH2 suggest that little if any coronary isomerase which converts endoperoxide into PGE2 exists, or that a novel, potent, PG-like substance is produced by the isolated coronary arteries. Although the coronaries do not possess thromboxane A2 synthetase activity, the vessels are profoundly contracted by exogenous thromboxane A2. Thromboxane A2 can be synthesized and released by circulating platelets when they are aggregated by endothelial injury or thrombin. Thus, coronary tone, and possible spasm, in ischemic myocardial zones may be influenced markedly by interplay between prostaglandins, endoperoxides, and thromboxane formed by platelets on the one hand, and endoperoxide products synthesized endogenously in the coronary arteries on the other.