A possible mechanism to explain how ischemia and maintained function of gastric type proton pumps could lead to hydrops of the inner ear in Meniere’s Disease.

A possible explanation of the genesis of Ménière's disease (MD) and other labyrinthine disorders on the basis of a direct involvement of the inner ear gastric type proton pump under ischaemia was recently outlined: maintained activity of the proton pump under acidic conditions could favour the onset of an endolymphatic hydrops through enhanced ion concentration in the endolymph and subsequent osmotic movement. The details of such a mechanism could be explained by considering the capability of sensory cells to extrude H+ into the endolymph in exchange for K+ through organellar isoforms that can transiently appear on plasma membranes and permit an electroneutral ion exchange. This capability appears to be rapidly activated under acidic conditions, which can be a consequence of a local ischaemia. This could mean that in an acidic milieu with an enhanced intracellular amount of H+, provided that the proton pumps maintain their activity as in other organs, a greater amount of K+ can finally be involved in the physiological cycling process and enter into the endolymph; this hypothesis seems reliable and could explain how an osmotic mechanism causing the onset of the hydrops could paradoxically be related to defensive responses to a vasospasm.