RationaleRecently, the efficacy of renal denervation (RDN) has been debated. It is discussed whether RDN is able to adequately target the renal nerves.ObjectiveWe aimed to investigate how effective RDN was by means of functional hemodynamic measurements and nerve damage on histology.Methods and ResultsWe performed hemodynamic measurements in both renal arteries of healthy pigs using a Doppler flow and pressure wire. Subsequently unilateral denervation was performed, followed by repeated bilateral hemodynamic measurements. Pigs were terminated directly after RDN or were followed for 3 weeks or 3 months after the procedure. After termination, both treated and control arteries were prepared for histology to evaluate vascular damage and nerve damage. Directly after RDN, resting renal blood flow tended to increase by 29±67% (P = 0.01). In contrast, renal resistance reserve increased from 1.74 (1.28) to 1.88 (1.17) (P = 0.02) during follow-up. Vascular histopathology showed that most nerves around the treated arteries were located outside the lesion areas (8±7 out of 55±25 (14%) nerves per pig were observed within a lesion area). Subsequently, a correlation was noted between a more impaired adventitia and a reduction in renal resistance reserve (β: -0.33; P = 0.05) at three weeks of follow-up.ConclusionOnly a small minority of renal nerves was targeted after RDN. Furthermore, more severe adventitial damage was related to a reduction in renal resistance in the treated arteries at follow-up. These hemodynamic and histological observations may indicate that RDN did not sufficiently target the renal nerves. Potentially, this may explain the significant spread in the response after RDN.
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.
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