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.
Keywords: Oxidative stress, Inflammation, DOCA-salt, cardiovascular remodelling, fibrosis, hypertrophy, pathophysiological stress state, Superoxide, cyclooxy-genases, myeloperoxidases, monooxygenase, thioredoxin, immune-inflammatory, uninephrectomised, randomized, extravasation, aldosteronism, min-eralocorticoid, vasoconstriction, mineralocorticoid, acetovanillone, Chronic, Aminoguanidine, acetylcholine, cyclo-oxygenase, chemotactic, suberoylanilide, pleiotropic, potential prolongation
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