Heart Care Info - Heart Disease Prevention & Treatment

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

H Tu, J Liu, Z Zhu, L Zhang... - Journal of ..., 2012 - Am Physiological Soc Abstract Our previous study has shown that chronic heart failure (CHF) reduces expression and activation of voltage-gated sodium (Na v) channels in baroreceptor neurons, which are involved in the blunted baroreceptor neuron excitability and contribute to the impairment ...

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 mitochondria-derived 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 (Mn SOD) and elevated the mitochondria-derived superoxide level in the nodose neurons compared with those in sham nodose neurons. Adenoviral Mn SOD (Ad.Mn SOD) gene transfection (50 multiplicity of infection) into the nodose neurons normalized the Mn SOD expression and reduced the elevation of mitochondrial superoxide in the nodose neurons from CHF rats. Ad.Mn SOD 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 Mn SOD and elevated mitochondria-derived superoxide, contributes to the reduced Nav channel activation and cell excitability in the aortic baroreceptor neurons in CHF rats.