Nitric oxide, oxidative stress and vascular endothelium in health and hypertension

Issue title: Selected Papers from 1st Meeting on “Cardiovascular Biology: Endothelial Cell in Health and Hypertension”, 30 June–1 July 2006, Prague, Czech Republic

Article type: Research Article

Authors: Rush, James W.E. | Ford, Rebecca J.

Affiliations: Department of Kinesiology, University of Waterloo, ON, Canada

Note: [] Corresponding author: James W.E. Rush, Department of Kinesiology, University of Waterloo, Waterloo, ON, Canada N2L 3G1. Tel.: +1 519 888-4567, ext. 2126; Fax: +1 519 885-0470; E-mail: [email protected].

Abstract: Oxidative stress contributes to homeostasis in vascular cells. However, excessive ROS is pathophysiological and contributes to impaired endothelium-dependent dilation in hypertension by decreasing NO bio-availability. NADPH oxidase is upregulated in hypertension by humoral and mechanical signals, and quantitatively this enzyme makes the largest contribution to ROS production. Genetic and chemical manipulation of NADPH oxidase and of antioxidant enzymes cause predictable changes in oxidative stress and endothelium-dependent function in hypertension. The chemical antioxidant glutathione also impacts endothelium-mediated vascular function, possibly through maintenance of S-nitrosothiols and via other independent antioxidant effects. The effects of changes in thiols and nitrosothiols on vasomotor function in hypertension need to be examined. H2O2 is believed to act as an EDHF physiologically. Thus, there must be competition between the influence of ROS and oxidative stress on NO-dependent dilation versus EDHF-dependent dilation. The crossover effects of ROS on the three main endothelium-dependent dilatory pathways must be examined in hypertension models.

Journal: Clinical Hemorheology and Microcirculation, vol. 37, no. 1-2, pp. 185-192, 2007