A new aspect in pathogenesis of experimental hydrops: role of calcium.

An imbalanced Ca++-homeostasis in the inner ear was demonstrated using an animal model for Menière's disease (MD). An increase of Ca++ concentration in the endolymph, as well as in some cells of the inner ear tissue, causes a rise of osmotic pressure and decrease of electric potential. Based on these results, we assume a new aspect in the pathophysiology of MD. It is proposed that the common denominator of MD, experimental endolymphatic hydrops (EEH), and space motion sickness (SMS) is primarily a shift of the inner ear Ca++ homeostasis towards a higher concentration of free Ca++ in the fluid compartments and adjacent intracellular spaces. It is postulated that an increase of Ca++ in this system might affect the transduction process and other functions associated with Ca++, such as turnover of otoconia.