Intrinsic prostaglandin release. A mediator of anoxia-induced relaxation in an isolated coronary artery preparation.
Isolated coronary artery strips of the bovine heart in vitro relax in response to decreased bath oxygen tensions (from 515 mm Hg to 112, 53, and 38 mm Hg). In addition, the rate of intrinsic formation and release of prostaglandin is considerably increased under conditions of decreased PO2. The vascular relaxations under reduced PO2 are attenuated and the elevations in prostaglandin output blocked by prostaglandin synthesis inhibitors. It appears that alterations in the output of a PGE with vasodilator activity, probably E1, is a significant factor regulating the compensatory changes in tone of the coronary arteries in response to anoxic conditions.
D015117:5,8,11,14-Eicosatetraynoic Acid / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000378:metabolism* / Q000503:physiopathology; D001241:Aspirin / Q000494:pharmacology; D002417:Cattle; D003331:Coronary Vessels / Q000378:metabolism* / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D007213:Indomethacin / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects; D010100:Oxygen / Q000494:pharmacology; D010313:Partial Pressure; D011453:Prostaglandins / Q000378:metabolism*; D012636:Secretory Rate / Q000187:drug effects; D013997:Time Factors
D011453:Prostaglandins; D015117:5,8,11,14-Eicosatetraynoic Acid; D001241:Aspirin; D010100:Oxygen; D007213:Indomethacin