Epithelial sodium channels contribute to the blunted sensitivity of aortic baroreceptors in chronic heart failure rats

Served as mechanosensor in mammalian nonepithelium, epithelial sodium channels (ENaC) are amiloride‐sensitive and voltage‐independent channels. They were found in the aortic baroreceptor cell bodies and terminals, and were thought to be components of the baroreceptor mechanosensitive channels. In addition, sensitivity of the aortic baroreceptors was depressed in chronic heart failure (CHF) animals. Therefore, we measured the expression of ENaC subunits in the nodose ganglion neurons and aortic baroreceptor terminals in sham and CHF rats. CHF was induced by left coronary artery ligation. The sensitivity of the aortic baroreceptors was blunted in anesthetized CHF rats, compared with that in sham rats. ¦Â and ¦Ã‐ENaC subunits were expressed in A‐type (myelinated) and C‐type (unmylinated) nodose neurons and aortic baroreceptor terminals but ¦Á‐ENaC subunit was not detected. CHF reduced protein levels of ¦Â and ¦Ã‐ENaC subunits in the nodose neurons and aortic baroreceptor terminals. In addition, using the whole cell patch‐clamp technique, we found that mechosensitive current density of the aortic baroreceptor neurons was lower in CHF rats than that in sham rats. These results suggest that reduced expression of ENaC channels is involved in the attenuation of aortic baroreceptor sensitivity, which subsequently contributes to the arterial baroreflex impairment in CHF state.