Abstract
Oxidative stress and inflammation are two sides of the same coin that are intricately combined to elicit a chronic pathophysiological stress state, especially as seen in cardiovascular remodelling. In this review, we argue that administration of deoxycorticosterone acetate (DOCA) and sodium chloride to uninephrectomised rats, defined as DOCA-salt hypertensive rats, provides a reliable animal model of oxidative and inflammatory stress in the cardiovascular system. The supporting evidence includes pathophysiological and biochemical changes together with pharmacological responses to synthetic and natural compounds that lower the concentrations of reactive free radical species and that curtail inflammatory responses in the cardiovascular system.
Highlights
Cardiovascular remodelling is the outcome of chronic pathophysiological stress in the cardiovascular system [1]
Over-expression of p47phox and gp91phox and reduced expression of intracellular superoxide dismutase have been reported with increased salt loading [52]. These findings suggest that NADPH oxidase is increased and is responsible for increased superoxide production and possibly contributes to the increased blood pressure in the deoxycorticosterone acetate (DOCA)-salt hypertensive rat [53]
Further evidence for a role of endothelin in the DOCA-salt model is provided by administration of an endothelin antagonist, which lowered blood pressure, and induced reversal of hypertrophic arterial remodelling [60], left ventricular fibrosis and inflammation [39, 40] and renal and cardiac hypertrophy [40]
Summary
Cardiovascular remodelling is the outcome of chronic pathophysiological stress in the cardiovascular system [1]. Inflammatory cells such as leukocytes increase expression and activity of pro-oxidant enzymes including myeloperoxidase and NADPH oxidases thereby aiding in the generation of excess reactive oxygen free radicals [4, 6]. Both oxidative stress mediated by reactive free radical species and inflammation following infiltration of immune-inflammatory cells are strongly implicated in inducing hypertension, hypertrophy, fibrosis, conduction abnormalities and endothelial dysfunc-
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