title: Renal denervation suppresses atrial fibrillation in a model of renal impairment.
abstract: BACKGROUND
  A close association exists between renal impairment (RI) and atrial fibrillation (AF) occurrence. Increased activity of the sympathetic nervous system (SNS) may contribute to the development of AF associated with RI. Renal denervation (RDN) decreases central sympathetic activity.
  
  
  OBJECTIVE
  The main objective of the study was to explore the effects of RDN on AF occurrence and its possible mechanisms in beagles with RI.
  
  
  METHODS
  Unilateral RI was induced in beagles by embolization of small branches of the renal artery in the right kidney using gelatin sponge granules in Model (n = 6) and RDN group (n = 6). The Sham group (n = 6) underwent the same procedure, except for embolization. Then animals in RDN group underwent radiofrequency ablation of the renal sympathetic nerve. Cardiac electrophysiological parameters, blood pressure, left ventricular end-diastolic pressure, and AF inducibility were investigated. The activity of the SNS, renin-angiotensin-aldosterone system (RAAS), inflammation and atrial interstitial fibrosis were measured.
  
  
  RESULTS
  Embolization of small branches of the renal artery in the right kidney led to ischemic RI. Heart rate, P wave duration and BP were increased by RI, which were prevented or attenuated by RDN. Atrial effective refractory period was shortened and AF inducibility was increased by RI, which were prevented by RDN. Antegrade Wenckebach point was shortened, atrial and ventricular rates during AF were increased by RI, which were attenuated or prevented by RDN. Levels of norepinephrine, renin and aldosterone in plasma, norepinephrine, angiotensin II, aldosterone, interleukin-6 and high sensitivity C-reactive protein in atrial tissue were elevated, and atrial interstitial fibrosis was enhanced by RI, which were attenuated by RDN.
  
  
  CONCLUSIONS
  RDN significantly reduced AF inducibility, prevented the atrial electrophysiological changes in a model of RI by combined reduction of sympathetic drive and RAAS activity, and inhibition of inflammation activity and fibrotic pathway in atrial tissue.
authors.affiliation: Department of Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Zhuo
authors.initials: Z
authors.lastname: Liang
authors.affiliation: Department of Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Xiang-min
authors.initials: XM
authors.lastname: Shi
authors.affiliation: Department of Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Li-feng
authors.initials: LF
authors.lastname: Liu
authors.affiliation: Department of Emergency, Beijing Tsinghua Changgeng Hospital Medical Center, Tsinghua University, Beijing, China.
authors.forename: Xin-pei
authors.initials: XP
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Zhao-liang
authors.initials: ZL
authors.lastname: Shan
authors.affiliation: Department of Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Kun
authors.initials: K
authors.lastname: Lin
authors.affiliation: Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Fu-kun
authors.initials: FK
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Yan-guang
authors.initials: YG
authors.lastname: Li
authors.affiliation: Department of Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Hong-Yang
authors.initials: HY
authors.lastname: Guo
authors.affiliation: Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Yu-tang
authors.initials: YT
authors.lastname: Wang
mesh_terms: D000450:Aldosterone / Q000032:analysis; D000804:Angiotensin II / Q000032:analysis; D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D017763:Autonomic Denervation / Q000379:methods; D002097:C-Reactive Protein / Q000032:analysis; D017115:Catheter Ablation; D004195:Disease Models, Animal; D004285:Dogs; D005355:Fibrosis; D006325:Heart Atria / Q000737:chemistry / Q000473:pathology; D006439:Hemodynamics; D015850:Interleukin-6 / Q000032:analysis; D007511:Ischemia / Q000150:complications / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery*; D007668:Kidney / Q000098:blood supply / Q000294:innervation*; D008955:Models, Cardiovascular; D009638:Norepinephrine / Q000032:analysis; D012077:Renal Artery / Q000473:pathology; D012078:Renal Artery Obstruction / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology
chemical_list: D015850:Interleukin-6; D000804:Angiotensin II; D000450:Aldosterone; D002097:C-Reactive Protein; D012083:Renin; D009638:Norepinephrine