Key result
In salt-sensitive hypertension, atherogenesis is closely linked to oxidative stress, and inhibiting Ang II or ROS prevents endothelial dysfunction independently of blood pressure in rat models.
Population
Hypertensive Dahl salt-sensitive rats (preclinical model of human salt-sensitive hypertension)
Design
Review
Authors
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Mechanisms of hypertension-driven atherosclerosis via endothelial dysfunction remain incompletely defined; leaves open relative hemodynamic versus vasoactive contributions.
In salt-sensitive hypertension, atherogenesis appears to be driven more by oxidative stress and local Angiotensin II activation than by hemodynamic stress alone, suggesting that antihypertensive therapy should target restoring the balance of vasoactive factors.
Schulman et al. (2006) conducted a review in Atherosclerosis and hypertension. Inhibition of Ang II type 1 receptor or NAD(P)H oxidase-derived ROS was evaluated. In salt-sensitive hypertension, atherogenesis is closely linked to oxidative stress, and inhibiting Ang II or ROS prevents endothelial dysfunction independently of blood pressure in rat models.
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