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Hypertension

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Studies on Renal Disorders

Abstract

Studies in animals have shown that oxidative stress precedes hypertension, and a variety of antioxidant treatments prevent or ameliorate genetic and acquired hypertension. Human studies have demonstrated deficiencies in several antioxidant mechanisms in patients with essential hypertension, but significant difficulties exist in designing conclusive therapeutic trials and a causal relationship between oxidative stress, and hypertension remains unproven. Increased intravascular pressure, shear, and oscillatory stress induce oxidative stress that results in a reduction in nitric oxide availability and endothelial dysfunction. In addition, oxidative stress activates kinases and phosphatases that induce vascular remodeling. The effects of reactive oxygen species on vascular tone are not uniform, but in the kidney they favor sodium retention. The mechanisms by which a high salt intake increases oxidative stress are reviewed. The interrelation between oxidative stress, inflammation, and angiotensin II activity in the kidney results in a tendency to sodium retention, which is the hallmark of salt-sensitive hypertension. The possible participation of a low-grade autoimmune reactivity in the kidney in the pathogenesis of essential hypertension is discussed.

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Rodriguez-Iturbe, B., Vaziri, N.D. (2011). Hypertension. In: Miyata, T., Eckardt, KU., Nangaku, M. (eds) Studies on Renal Disorders. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press. https://doi.org/10.1007/978-1-60761-857-7_7

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