O Papel do Rim, Renina e Estresse Oxidativo no Desenvolvimento da Hipertensão Essencial (Inglês)

In this review we intend to examine the possibility that small increments of angiotensin II could be responsible for an increase in blood pressure and maintenance of hypertension through the stimulation of oxidative stress. It has been shown that a low dose of angiotensin II (2-10 ng/kg/min), which does not elicit an immediate pressor response, when given for 7-30 days by continuous intravenous infusion, can increase mean arterial pressure by 30-40 mmHg. This slow pressor response to angiotensin is accompanied by the stimulation of oxidative stress as measured by a significant increase in 8-iso-PGF2? (F2-isoprostanes), which has been hypothesized to be produced by the chemical combination of superoxide radicals and nitric oxide to form peroxynitrite which can then oxidize arachidonic acid to form F2-isoprostanes. F2-isoprostanes exert potent vasoconstrictor and antinatriuretic effects. Furthermore, angiotensin II can stimulate endothelin production which has been shown to also stimulate oxidative stress. In this way a reduction in the concentration of nitric oxide (being quenched by superoxide) along with the formation of F2-isoprostanes and endothelin could potentiate the vasoconstrictor effects of angiotensin II. We hypothesize that these mechanisms which underlie the development of the slow pressor response to angiotensin II also participate in the production ...

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