Published online before print September 18, 2006, doi: 10.1161/01.HYP.0000242338.42238.d6
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(Hypertension. 2006;48:826.)
© 2006 American Heart Association, Inc.
Editorial Commentary |
Heme Oxygenase-1 Inhibition of Nox Oxidase Activation Is a Microvascular Endothelial Antioxidant Effect of NO
From the Departments of Physiology (M.S.W.) and Pharmacology (N.G.A.), New York Medical College, Valhalla, NY.
Correspondence to Michael S. Wolin, Department of Physiology, Basic Science Bldg, Room 604, New York Medical College, Valhalla, NY 10595. E-mail mike_wolin@nymc.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
A study by Jiang et al1 in this issue of Hypertension reports evidence suggesting that NO has a novel antioxidant-type effect in cultured human microvascular endothelial cells associated with an inhibition of Nox oxidase activation, which seems to be mediated by increasing the expression and activity of heme oxygenase-1 (HO-1). The induction of HO-1 was observed to occur when the cultured endothelium was exposed to a long-acting NO donor for 
6 hours. Because freshly isolated vascular tissue from normal animals is generally thought to contain low levels of HO-1, the levels of NO seen in endothelium under physiological conditions do not seem to be a stimulus for maintaining an elevated level of this enzyme.
Physiological stresses associated with oxidant production were initially observed to increase HO-1 expression in multiple tissue preparations.2 The formation of reactive NO-derived species (NOx) from the reaction of NO with superoxide, such as peroxynitrite, were initially observed to promote HO-1 expression in endothelial cells exposed to NO donors in a manner that was modulated by free thiol availability.3 Although the precise mechanism involved in how NOx induces HO-1 expression is currently not known, the gene for HO-1 has many sites in its promoter region for redox regulation by intracellular and nuclear signaling events that lead to transcriptional activation.2 Thus, increases in HO-1 expression by elevated levels of NO are likely to occur when endothelium is exposed to physiological stress or pathophysiological conditions associated with vascular disease processes, such as hypertension.
The decreased detection of superoxide
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Hypertension 2006 48: 950-957.
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