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Cardiovascular Research 2000 45(1):148-155; doi:10.1016/S0008-6363(99)00316-8
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Inducible nitric oxide synthase and cardiovascular disease

Ajay M Shah*

Department of Cardiology, GKT School of Medicine, King's College London, UK

* Tel.: +44-171-346-3106; fax: +44-171-346-3685

KEYWORDS Adenosine; Arrhythmia (mechanisms); Contractile function; Ischemia; Preconditioning; Reperfusion

The first 150 words of the full text of this article appear below.


   1 Introduction
 
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].


   2 Historical account
 
Appreciation of the role of NO in the cardiovascular system dates back to 1980 and the seminal . . . [Full Text of this Article]


   3 NO in the cardiovascular system
 

   4 In vitro expression and effects of iNOS
 

   5 Role of iNOS in vivo: General considerations
 

   6 iNOS and endotoxic shock – vascular dysfunction and mortality
 

   7 iNOS and endotoxic shock – myocardial dysfunction
 

   8 Role of iNOS in other cardiovascular disorders
 
8.1 Myocarditis
8.2 Dilated cardiomyopathy and heart failure
8.3 Cardiac allograft rejection

   9 Conclusions
 

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[Abstract] [Full Text] [PDF]