ABSTRACT
The sudden removal of oxygen (anoxia) augments contractile responses in isolated canine peripheral, coronary, and cerebral arteries. In “sandwich” preparations of the canine coronary artery contracted with prostaglandin F2α, the hypoxic facilitation can be transferred from a donor tissue with endothelium to a coronary artery strip without endothelium demonstrating that the hypoxic endothelium releases a diffusible contracting factor. Exogenous arachidonic acid induces endothelium-dependent contractions in canine veins. The response can be blocked by inhibitors of cyclooxygenase, but not those of prostacyclin or thromboxane synthetase. In certain blood vessels, endothelium-dependent contractions involving the metabolism of arachidonic acid can be evoked with agonists which under most circumstances evoke endothelium-dependent relaxations of other blood vessels. Thus, in the aorta of the spontaneously hypertensive rat, the renal artery of the normal rat, and in the basilar artery of dog and rabbit, acetylcholine induces endothelium-dependent contractions which can be blocked by indomethacin.
