THE EFFECT OF NIMODIPINE ON COCHLEAR POTENTIALS AND NA+ K+-ATPASE ACTIVITY IN NORMAL AND HYDROPIC COCHLEAS OF THE ALBINO GUINEA-PIG/

In experimental endolymphatic hydrops (EEH) a decrease in the endococh lear potential (EP) has been reported and is thought to be due to decr eased activity of the enzyme Na+/K+-ATPase in the stria vascularis. By stimulating Na+/K+-ATPase, the EP, and thereby cochlear function as a whole, might be restored. On the other hand, stimulation of stria vas cularis Na+/K+-ATPase might result in excessive production of endolymp h and thus produce or augment hydrops. In this study we have investiga ted the effect of intraperitoneaIly applied nimodipine on cochlear pot entials and on Na+/K+-ATPase activity in the stria vascularis, both in normal cochleas (control) and in cochleas with EEH. Nimodipine is an L-type Ca2+-channel blocking agent with Na+/K+-ATPase stimulating prop erties at concentrations as low as 1.5 mM. The compound action potenti al (CAP), evoked by 2, 4 and 8 kHz tone bursts was found to be depress ed in the EEH ears with and without nimodipine treatment, and in the n imodipine treated control ears. Statistical analysis (ANOVA) showed th at the effects of EEH and nimodipine on the CAP were additive. The neg ative summating potential (SP), measured extracochlearly at the apex, in response to 4 and 8 kHz tone bursts was significantly enhanced in t he EEH ears. Nimodipine treatment did not affect the SP, neither in th e control, nor in the EEH ears. Cytochemically, Na+/K+-ATPase activity appeared to be decreased in the oedematous stria vascularis of hydrop ic cochleas. No effect of nimodipine on Na+/K+-ATPase activity could b e established ultracytochemically, neither in the controls nor in the EEH ears. In the lower turns of some of the nimodipine treated control cochleas a mild hydrops was seen during light-microscopic evaluation. Although it was not possible to prove a stimulatory effect of nimodip ine on the enzyme Na+/K+-ATPase cytochemically, the finding of mild en dolymphatic hydrops in nimodipine treated control ears suggests (a his tory of) increased endolymph production. This hydrops might be respons ible for the depression of the CAP in the nimodipine treated ears.