The experiments on 18 guinea pigs were divided into two groups and each group was arranged in such a way that the effect of hypercapnia (generated by breathing 10% CO2-90% O2) was investigated with and without inhibition of carbonic anhydrase by methazolamide, 25 mg/kg, in the first group and acetazolamide, 50 mg/kg, in the second group, administered intravenously. The endocochlear potentials (EP) and endocochlear PO2 were recorded by microelectrodes introduced into the scala media, and cochlear microphonics (CM) were monitored by a silver-wire electrode from the round window. In the first exposure to hypercapnia (20-40 min) EP increased about + 6 mV. At the same time CM decreased; the reason for this is not yet known. During the second period of hypercapnia (80-100 min) when carbonic anhydrase was inhibited with methazolamide and acetazolamide, EP did not elevate as during the first period when carbonic anhydrase was not inhibited. In this work, under specific conditions, it was observed for the first time that carbonic anhydrase affects the generation of EP.