Abstract
Furosemide-induced changes of cochlear potentials were used as a model to study the influence of arachidonic acid metabolites on ion movements within the cochlea. No influence was exerted by the drugs Esculetin — blocking the synthesis of lipoxygenase products — and Dazoxiben — suppressing thromboxane A 2 levels within the cochlea. A weakening of the furosemide-induced changes of the endocochlear potential was found when infusing the thromboxane (TX) receptor antagonists BM 13 505 and BM 13 177 before furosemide was given. This effect was also observed when pre-treating the guinea pig with a specific platelet-activating factor receptor antagonist, BN 52 021, before the diuretics was given. Summating potential and cochlear microphonics remained insignificantly changed against controls. The results suggest that a TX receptor contributes to the control of ion movements within the cochlea. A possible involvement of loop diuretics' receptors is discussed.
Published Version
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