title: Altered ENaC is Associated With Aortic Baroreceptor Dysfunction in Chronic Heart Failure.
abstract: BACKGROUND
  Abnormal baroreceptor function contributes to attenuated arterial baroreflex sensitivity in chronic heart failure (CHF). As a mechanosensor in mammalian nonepithelium, the epithelial sodium channel (ENaC) is an amiloride-sensitive and voltage-independent ion channel. The ENaC is thought to be a component of baroreceptor mechanosensitive ion channels in aortic baroreceptor cell bodies and nerve terminals. In this study, therefore, we measured the expression and activation of the ENaC in nodose neuronal cell bodies and aortic baroreceptor nerve terminals in sham and CHF rats.
  
  
  RESULTS
  CHF was induced by surgical ligation of left coronary artery. The development of CHF was confirmed by hemodynamic and morphological characteristics. The aortic baroreceptor sensitivity was blunted in anesthetized CHF rats, compared with that in sham rats. The data from immunostaining and western blot analysis showed that the protein of β- and γ-ENaC subunits was expressed in nodose neuronal cell bodies and aortic baroreceptor nerve terminals, whereas the protein of α-ENaC subunit was undetectable. CHF reduced protein expression of β- and γ-ENaC subunits in nodose neuronal cell bodies and aortic baroreceptor nerve terminals. Additionally, the data recorded by the whole cell patch-clamp technique demonstrated that ENaC currents in aortic baroreceptor neurons were lower in CHF rats than that in sham rats.
  
  
  CONCLUSIONS
  These results suggest that reduced protein expression of the ENaC decreases the ENaC activation, which could be involved in attenuation of the aortic baroreceptor sensitivity in the CHF state. Baroreceptors should be a potential therapeutic target for reducing mortality in CHF.
authors: Department of Emergency Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA; Department of Cellular and integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska, USA. yulongli@unmc.edu.
authors: Yu-Long
authors: YL
authors: Li
authors: Department of Emergency Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA;
authors: Dongze
authors: D
authors: Zhang
authors: Department of Emergency Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA;
authors: Huiyin
authors: H
authors: Tu
authors: Department of Emergency Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA;
authors: Robert L
authors: RL
authors: Muelleman
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism* / Q000503:physiopathology; D017704:Baroreflex; D002908:Chronic Disease; D004195:Disease Models, Animal; D015536:Down-Regulation; D053503:Epithelial Sodium Channels / Q000378:metabolism*; D006333:Heart Failure / Q000378:metabolism* / Q000503:physiopathology; D006439:Hemodynamics; D008297:Male; D040542:Mechanotransduction, Cellular; D008564:Membrane Potentials; D009620:Nodose Ganglion / Q000378:metabolism* / Q000503:physiopathology; D011311:Pressoreceptors / Q000378:metabolism* / Q000503:physiopathology; D017729:Presynaptic Terminals / Q000378:metabolism; D017207:Rats, Sprague-Dawley
chemical_list: D053503:Epithelial Sodium Channels; C507050:Scnn1b protein, rat; C507054:Scnn1g protein, rat
keywords: ENaC; baroreceptor; blood pressure; electrophysiology; heart failure; hypertension.