Dependence of endocochlear potential on vascular pH.

The vasculature of the inner ear was perfused with simple salt solutions which were buffered with HCO3/CO2, PO4 or Hepes (N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid). Replacement of HCO3/CO2 with either PO4 or Hepes at constant pH led to a rapid decline of about 15 mV in the endocochlear potential (EP) to a new steady-state level which could be maintained for over 30 min. This effect was reversible. Changes in [HCO3] over a wide range (nominally 0-100 mM) at constant CO2 tension produced only small (less than 3 mV) changes in the EP. However, the EP declined markedly when [HCO3] was maintained constant at 25 mM while CO2 tension was lowered. The response to increased CO2 was more complex. Additional experiments were performed in which intracellular pH was presumably altered by vascular perfusion of NH4 (alkalinization), or propionate (acidification). Perfusion of ammonium led to a strong decline of the EP (-38.2 +/- 2.5 S.D.) while propionate produced a small positive shift of about 3-4 mV. Acetazolamide (1 mM) decreased the EP by 7.6 +/- 2.7 mV and 14.8 +/- 4.6 mV in HCO3/CO2 and Hepes medium, respectively, after 10 min perfusion; this effect was poorly reversible. These results suggest that intracellular pH has a strong influence on the level of EP and further demonstrate that vascular [HCO3] and pH are not critical parameters for generation of the EP.