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Vol. 29, Issue 11, 1366-1376, November 2001
Targets and Sources
of Nitric Oxide
Department of Pharmacology, Emory University School of
Medicine, Atlanta, Georgia (E.T.M.); Department of Biology, University
of Konstanz, Konstanz, Germany (V.U., A.D., P.S.); Institute of Applied
Biochemistry, University of Tsukuba, Ibaraki, Japan (N.T.); Department
of Biotechnology, University of Tokyo, Tokyo, Japan (H.S.); Department
of Pharmacology, New York Medical College, Valhalla, New York
(J.C.McG.); Center for Cardiovascular Diseases, Texas Southern
University, Houston, Texas (A.O.); Department of Pharmacology and
Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin (C.J.H.,
W.B.C); Department of Pharmacology and Toxicology, Inha University,
Incon, Korea (C.S.P., H.G.Y., Y.N.C.); Department of Pharmacology,
Hanyang University, Seoul, Korea (J.S.K.); and UMR 8601 Centre National
de la Recherche Scientifique, University of Paris V, Paris, France
(D.M., J.-L. B.).
This article is a report on a symposium sponsored by the American
Society for Pharmacology and Experimental Therapeutics and held at the
Experimental Biology 01 meeting in Orlando, FL. The presentations
addressed the mechanisms of inhibition and regulation of cytochrome
P450 and flavin monooxygenase enzymes by nitric oxide. They also
highlighted the consequences of these effects on metabolism of drugs
and volatile amines as well as on important physiological parameters,
such as control of blood pressure, renal ion transport, and
steroidogenesis. This is achieved via regulation of P450-dependent
prostacyclin, hydroxyeicosatetraenoic acid, and epoxyeicosatrienoic
acid formation. Conversely, the mechanisms and relative importance of
nitric oxide synthases and P450 enzymes in NO production from
endogenous and synthetic substrates were also addressed.
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