ENaC subunits are molecular components of the arterial baroreceptor complex

Abstract

Mechanosensation is essential to the perception of our environment. It is required for hearing, touch, balance, proprioception, and blood pressure homeostasis. Yet little is known about the identity of ion-channel complexes that transduce mechanical stimuli into neuronal responses. Genetic studies in Caenorhabditis elegans suggest that members of the DEG/ENaC family may be mechanosensors. Therefore we tested the hypothesis that mammalian epithelial Na+-channel (ENaC) subunits contribute to the mechanosensor in baroreceptor neurons. The data presented here show that ENaC transcripts and proteins are expressed in mechanosensory neurons and at the putative sites of mechanotransduction in baroreceptor sensory-nerve terminals. Additionally, known ENaC inhibitors, amiloride and benzamil, disrupt mechanotransduction in arterial baroreceptor neurons. These data are consistent with the hypothesis that DEG/ENaC proteins are components of mechanosensitive ion-channel complexes.