Renal denervation based on experimental rationale

Kenichi Katsurada, Yukako Ogoyama, Yasushi Imai, Kaushik P. Patel, Kazuomi Kario

Research output: Contribution to journalReview articlepeer-review

14 Scopus citations

Abstract

Excessive activation of the sympathetic nervous system is one of the pathophysiological hallmarks of hypertension and heart failure. Within the central nervous system, the paraventricular nucleus (PVN) of the hypothalamus and the rostral ventrolateral medulla in the brain stem play critical roles in the regulation of sympathetic outflow to peripheral organs. Information from the peripheral circulation, including serum concentrations of sodium and angiotensin II, is conveyed to the PVN via adjacent structures with a weak blood–brain barrier. In addition, signals from baroreceptors, chemoreceptors and cardiopulmonary receptors as well as afferent input via the renal nerves are all integrated at the level of the PVN. The brain renin-angiotensin system and the balance between nitric oxide and reactive oxygen species in these brain areas also determine the final sympathetic outflow. Additionally, brain inflammatory responses have been shown to modulate these processes. Renal denervation interrupts both the afferent inputs from the kidney to the PVN and the efferent outputs from the PVN to the kidney, resulting in the suppression of sympathetic outflow and eliciting beneficial effects on both hypertension and heart failure.

Original languageEnglish
Pages (from-to)1385-1394
Number of pages10
JournalHypertension Research
Volume44
Issue number11
DOIs
StatePublished - Nov 2021
Externally publishedYes

Keywords

  • Heart failure
  • Hypertension
  • Paraventricular nucleus
  • Renal denervation
  • Sympathetic nervous system

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