Mechanism of vasodilation during and after ischemic exercise.
This article reviews work on the cause of the vasodilation associated with exercise in the absence of sufficient blood flow. This situation results in a prolonged period of vasodilation that far exceeds the time required for muscle oxygen consumption (VO2) to return to rest. This prolonged vasodilation is not caused by release of K+ or lactic acid, hyperosmolarity, or lowered vessel wall pO2. The early portion appears to be caused by adenosine release, because tissue adenosine is elevated and theophylline partly blocks the response. The remainder may be caused by prostaglandin release which is elevated late in the post-exercise vasodilation period. Indomethacin reduces the duration of the vasodilation. Histamine may play a role in the vasodilation because tripelennamine reduces it. The vasodilation during the exercise bout is probably the result of at least three factors. K+ release and hyperosmolarity probably help to initiate the vasodilation and adenosine probably becomes the dominant factor after the first 10--20 minutes.
D000241:Adenosine / Q000378:metabolism*; D000818:Animals; D004285:Dogs; D005552:Forelimb / Q000098:blood supply; D007213:Indomethacin / Q000494:pharmacology; D007511:Ischemia / Q000097:blood / Q000503:physiopathology*; D005082:Physical Exertion; D011458:Prostaglandins E / Q000097:blood*; D014309:Tripelennamine / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D011458:Prostaglandins E; D014309:Tripelennamine; D000241:Adenosine; D007213:Indomethacin