Abstract：
:To determine the mechanism of anoxic vasoconstriction, precontracted rat aortic rings were exposed to 95% N2, which caused additional contraction. Reoxygenation (95% O2) resulted in initial relaxation followed by contraction. Indomethacin did not affect anoxic contraction or reoxygenation-mediated events, but NG-monomethyl-1-arginine, which inhibits EDRF synthesis, and oxyhemoglobin, which reduces EDRF activity, markedly decreased anoxic contraction and reoxygenation relaxation, and potentiated subsequent contraction. Superoxide dismutase did not affect anoxic contraction, but potentiated reoxygenation relaxation and attenuated subsequent contraction. Endothelin concentrations remained unchanged throughout anoxia and reoxygenation. Thus, anoxic contraction and reoxygenation-mediated early relaxation appear to be due to changes in EDRF. On the other hand, reoxygenation-induced contraction appears related to release of superoxide radicals.
journal_name
Life Scijournal_title
Life sciencesauthors
Mehta JL,Lawson DL,Yang BC,Haught WH,Hintze Tdoi
10.1016/0024-3205(91)90316-4subject
Has Abstractpub_date
1991-01-01 00:00:00pages
1739-46issue
23eissn
0024-3205issn
1879-0631pii
0024-3205(91)90316-4journal_volume
49pub_type
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