Mitochondria-derived superoxide and voltage-gated sodium channels in baroreceptor neurons from chronic heart-failure rats

Huiyin Tu, Jinxu Liu, Zhen Zhu, Libin Zhang, Iraklis I. Pipinos, Yu Long Li

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

Our previous study has shown that chronic heart failure (CHF) reduces expression and activation of voltage-gated sodium (Nav) channels in baroreceptor neurons, which are involved in the blunted baroreceptor neuron excitability and contribute to the impairment of baroreflex in the CHF state. The present study examined the role of mitochondriaderived superoxide in the reduced Nav channel function in coronary artery ligation-induced CHF rats. CHF decreased the protein expression and activity of mitochondrial complex enzymes and manganese SOD (MnSOD) and elevated the mitochondria-derived superoxide level in the nodose neurons compared with those in sham nodose neurons. Adenoviral MnSOD (Ad.MnSOD) gene transfection (50 multiplicity of infection) into the nodose neurons normalized the MnSOD expression and reduced the elevation of mitochondrial superoxide in the nodose neurons from CHF rats. Ad.MnSOD also partially reversed the reduced protein expression and current density of the Nav channels and the suppressed cell excitability (the number of action potential and the current threshold for inducing action potential) in aortic baroreceptor neurons from CHF rats. Data from the present study indicate that mitochondrial dysfunction, including decreased protein expression and activity of mitochondrial complex enzymes and MnSOD and elevated mitochondria-derived superoxide, contributes to the reduced Nav channel activation and cell excitability in the aortic baroreceptor neurons in CHF rats.

Original languageEnglish (US)
Pages (from-to)591-602
Number of pages12
JournalJournal of Neurophysiology
Volume107
Issue number2
DOIs
StatePublished - Jan 1 2012

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Keywords

  • Adenoviral vector
  • Manganese superoxide dismutase

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology

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