Different mechanisms of hypoxic relaxation in canine coronary arteries and rat abdominal aortas.

Hypoxia causes complex changes in vascular tone of isolated blood vessels. This study was performed in rings with and without endothelium of rat abdominal aortas and canine coronary arteries suspended in organ chambers for isometric tension recording. In both aortic and coronary rings with endothelium precontracted with a half-maximal concentration of phenylephrine or prostaglandin F2 alpha, respectively, hypoxia induced transient relaxations (20 +/- 2 and 15 +/- 3%, respectively); removal of the endothelium prevented the response in aortas, but not coronary arteries. The transient hypoxic relaxation was followed in both preparations by endothelium-dependent contractions (EDCs). Hypoxic relaxations were prevented by indomethacin (10 microM) in canine arteries, but not in rat aortas. The inhibitor of nitric oxide (NO) synthase, N omega-nitro-L-arginine (30 microM), inhibited hypoxic relaxations in intact rat aortas, but left those in coronary arteries unchanged. Similar results were obtained with methylene blue and LY 83583. In preparations without endothelium, sodium nitroprusside (30 nM) elicited a reappearance of hypoxic relaxations in the rat but not the dog coronary artery. Thus, hypoxic relaxation is mediated by a prostaglandin in the dog coronary artery, but by endothelium-derived NO in the rat aorta. As the response was dependent on the level of contraction, this suggests that the release or action of NO decreases with increasing tone.