Why the study?
Does reducing brain oxidative stress lower blood pressure and sympathetic nervous system activity in hypertensive rat models?
Does reducing brain oxidative stress lower blood pressure and sympathetic nervous system activity in hypertensive rat models?
Oxidative stress in the brain's vasomotor center is a key driver of sympathetic overactivity in hypertension, representing a potential therapeutic target for centrally acting drugs like ARBs.
Should not yet change hypertension practice; extends preclinical support for central oxidative stress as a target.
Oxidative stress is a key factor in the pathogenesis of hypertension and target organ damage, beginning in the earliest stages. Extensive evidence indicates that the pivotal role of oxidative stress in the pathogenesis of hypertension is due to its effects on the vasculature in relation to the development of atherosclerotic processes. It remains unclear, however, whether oxidative stress in the brain, particularly the autonomic nuclei (including the vasomotor center), has an important role in the occurrence and maintenance of hypertension via activation of the sympathetic nervous system. The aim of the present review is to describe the contribution of oxidative stress in the brain to the neural mechanisms that underlie hypertension, and discuss evidence that brain oxidative stress is a potential therapeutic target.
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Hirooka et al. (2010) studied this question.
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