Effects of some vasodilating (dipyridamole, nifedipine and verapamil) and antihypertensive (propranolol, hydralazine) drugs on arachidonic acid metabolism in isolated rat aorta and lung have been studied. Dipyridamole significantly increased the formation of PGI2 in aorta and lung. Nifedipine and verapamil decreased the formation of PGI2 in aorta, these drugs though significantly increased the formation of PGI2 in lung. Nifedipine showed no appreciable effect on the generation of TxA2 in rat aorta but in lung both nifedipine and verapamil reduced TxA2 formation though significantly only in the latter case. Dipyridamole showed no effect. The beneficial effect of dipyridamole, seems, at least in part, to be due to its ability to enhance the production of PGI2 both in the aorta and lung, and probably in other tissues as well. Nifedipine and verapamil may show their antianginal effect by a combined effect of enhanced PGI2 and reduced TxA2 formation in lung. In lung, whereas hydralazine reduced the formation of both PGI2 and TxA2, propranolol increased the formation of PGI2. Hydralazine reduced the formation of TxA2 and increased PGI2 formation in aorta. The effect of the drugs on the ability of rat aorta to inhibit collagen induced platelet aggregation of human blood platelets was also examined.