Oxidative Stress in Arterial Hypertension: Role of NAD(P)H Oxidase
Palabras clave : 
Angiotensin II
Genetics
Hypertension arterial
Stress
Free radicals
Fecha de publicación: 
2001
Editorial : 
American Heart Association
ISSN: 
1524-4563
Cita: 
Zalba G, San José G, Moreno MU, Fortuño MA, Fortuño A, Beaumont FJ, et al. Oxidative stress in arterial hypertension: role of NAD(P)H oxidase. Hypertension 2001 Dec 1;38(6):1395-1399.
Resumen
Increased vascular reactive oxygen species production, especially superoxide anion, contributes significantly in the functional and structural alterations present in hypertension. An enhanced superoxide production causes a diminished NO bioavailability by an oxidative reaction that inactivates NO. Exaggerated superoxide levels and a low NO bioavailability lead to endothelial dysfunction and hypertrophy of vascular cells. It has been shown that the enzyme NAD(P)H oxidase plays a major role as the most important source of superoxide anion in vascular cells. Several experimental observations have shown an enhanced superoxide generation as a result of the activation of vascular NAD(P)H oxidase in hypertension. Although this enzyme responds to stimuli such as vasoactive factors, growth factors, and cytokines, some recent data suggest the existence of a genetic background modulating the expression of its different components. New polymorphisms have been identified in the promoter of the p22(phox) gene, an essential subunit of NAD(P)H oxidase, influencing the activity of this enzyme. Genetic investigations of these polymorphisms will provide novel markers for determination of genetic susceptibility to oxidative stress in hypertension.

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Fichero: 
2001 Zalba Review Hypertension.pdf
Descripción: 
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222,55 kB
Formato: 
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