Inducible nitric oxide synthase and cardiovascular disease.
Open Access
- 1 January 2000
- journal article
- editorial
- Published by Oxford University Press (OUP) in Cardiovascular Research
- Vol. 45 (1) , 148-155
- https://doi.org/10.1016/s0008-6363(99)00316-8
Abstract
The simple gas nitric oxide (NO) has a diverse array of actions in numerous physiological and pathophysiological processes in the cardiovascular system. Three distinct NO synthase (NOS) isoforms, each encoded for by separate genes, have now been identified [1–4]. nNOS (or ‘neuronal’ NOS, NOS1) and eNOS (or ‘endothelial’ NOS, NOS3) are constitutive, Ca2+-regulated isoforms expressed not only in nervous tissue and endothelium respectively, but also in several other cell types. iNOS (or NOS2) can be expressed in almost any cell type upon appropriate stimulation. All NOS isoforms can be transcriptionally and post-transcriptionally regulated [5]. The generation of NO requires l-arginine, O2, NADPH, and tetrahydrobiopterin (BH4). In situations where there is l-arginine and/or BH4 deficiency, all the NOSs can generate superoxide as well as NO [6].Keywords
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