Vascular pH

1. Hear Res. 1987 Nov;31(1):1-7.

Dependence of endocochlear potential on vascular pH.

Arakawa E(1), Marcus DC, Thalmann R.

Author information:

(1)Washington University, Dept. of Otolaryngology, St. Louis, Missouri 63110.

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.

PMID: 3429347  [PubMed - indexed for MEDLINE]