Dependence of endocochlear potential on vascular pH.

The inner ear's endocochlear potential (EP) is a key factor in auditory transduction. Prior research has shown that vascular perfusion with HCO3/CO2 solutions influences EP. However, the exact role of pH and bicarbonate in EP remains unclear. This gap motivated further investigation into how vascular perfusion affects EP. Earlier studies suggested that pH and bicarbonate levels might be linked to EP stability. Yet, no prior work had resolved whether pH changes alone could alter EP. The current study addresses this uncertainty by testing perfusion with different buffers. These experiments aim to clarify the relationship between vascular pH and EP dynamics.

This study aimed to determine how vascular perfusion with different buffers affects the endocochlear potential. The specific problem addressed was whether pH or bicarbonate levels are critical for EP maintenance. The motivation came from prior findings that EP is sensitive to buffer changes. The authors sought to isolate the role of pH from other variables. They tested perfusion with HCO3/CO2, PO4, and Hepes buffers. They also examined the impact of altering intracellular pH via ammonium or propionate. The goal was to assess whether vascular pH directly influences EP. This approach allows for a clearer understanding of EP regulation mechanisms.

The inner ear vasculature was perfused with salt solutions buffered with HCO3/CO2, PO4, or Hepes. The perfusion solutions were adjusted to maintain constant pH while varying bicarbonate levels. Intracellular pH was altered using ammonium or propionate perfusion. The EP was measured before and after buffer or pH changes. The experiments tracked EP changes over time following buffer replacement. The perfusion was maintained for up to 30 minutes to observe steady-state effects. Acetazolamide was introduced to assess its impact on EP. The study focused on the reversibility of EP changes after buffer or pH adjustments.

Replacing HCO3/CO2 with PO4 or Hepes at constant pH caused a 15 mV decline in EP. This decline was reversible and could be sustained for over 30 minutes. Changing bicarbonate concentration at constant CO2 had minimal effect on EP. Lowering CO2 tension while keeping bicarbonate constant caused a marked EP decline. Ammonium perfusion led to a significant EP decrease of -38.2 mV. Propionate perfusion caused a small EP increase of 3-4 mV. Acetazolamide reduced EP by 7.6 mV in HCO3/CO2 and 14.8 mV in Hepes. These effects were poorly reversible after 10 minutes of perfusion.

The authors propose that intracellular pH strongly influences EP levels. They suggest that vascular bicarbonate and pH are not essential for EP generation. The findings indicate that pH changes, rather than bicarbonate concentration, affect EP. The reversibility of EP changes supports a dynamic pH-dependent mechanism. Ammonium perfusion had a more pronounced effect than propionate. Acetazolamide's impact varied with buffer type, suggesting a complex interaction. These results align with the hypothesis that pH regulation is central to EP modulation. The study highlights the need for further investigation into pH-dependent mechanisms.