Ischemia and reactive oxygen species in sympathetic hyperactivity states: a vicious cycle that can be interrupted by renal denervation?

Abstract

Renal denervation has developed as a new treatment strategy for patients suffering from resistant hypertension. The success of this therapy is due to the fact that sympathetic hyperactivity is involved in the pathogenesis of elevated blood pressure. However, not only the sympathetic nervous system (SNS), but also the renin angiotensin system (RAS) is known to be involved in hypertension. In addition, RAS is involved in other sympathetic hyperactivity states, such as heart failure, chronic kidney disease, insulin resistance and obstructive sleep apnea. Moreover, renal denervation has a beneficial effect on patients suffering from these disease states. Recent research suggested that the production of reactive oxygen species (ROS) is elevated in sympathetic hyperactivity states, and that ROS are able to activate the SNS and local tissue renin angiotensin system. Therefore, this review discusses the possibility of ROS as a common trigger of SNS and RAS activity in sympathetic hyperactivity states, and the effect of renal denervation on this ROS production.