title: Effects of CO2/HCO3- in perilymph on the endocochlear potential in guinea pigs.
abstract: The effect of CO(2)/HCO(3)(-) on the endocochlear potential (EP) was examined by using both ion-selective and conventional microelectrodes and the endolymphatic or perilymphatic perfusion technique. The main findings were as follows: (i) A decrease in the EP from approximately +75 to approximately +35 mV was produced by perilymphatic perfusion with CO(2)/HCO(3)(-)-free solution, which decrease was accompanied by an increase in the endolymphatic pH (DeltapH(e), approximately 0.4). (ii) Perilymphatic perfusion with a solution containing 20 mM NH(4)Cl produced a decrease in the EP (DeltaEP, approximately 20 mV) with an increase in the pH(e) (DeltapH(e), approximately 0.2), whereas switching the perfusion solution from the NH(4)Cl solution to a 5% CO(2)/25 mM HCO(3)(-) solution produced a gradual increase in the EP to the control level with the concomitant recovery of the pH(e). (iii) The perfusion with a solution of high or low HCO(3)(-) with a constant CO(2) level within 10 min produced no significant changes in the EP. (iv) Perfusion of the perilymph with 10 microg/ml nifedipine suppressed the transient asphyxia-induced decrease in EP slightly, but not significantly. (v) By contrast, the administration of 1 microg/ml nifedipine via the endolymph inhibited significantly the reduction in the EP induced by transient asphyxia or perilymphatic perfusion with CO(2)/HCO(3)(-)-free or 20 mM NH(4)Cl solution. These findings suggest that the effect of CO(2) removal from perilymphatic perfusion solution on the EP may be mediated by an increase in cytosolic Ca(2+) concentration induced by an elevation of cytosolic pH in endolymphatic surface cells.
authors.affiliation: Department of Physiology, Osaka Medical College, Osaka, 569-8686, Japan.
authors.forename: Yoshitsugu
authors.initials: Y
authors.lastname: Nimura
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Mori
authors.forename: Takaki
authors.initials: T
authors.lastname: Inui
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Sohma
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Takenaka
authors.forename: Takahiro
authors.initials: T
authors.lastname: Kubota
mesh_terms: D000643:Ammonium Chloride / Q000378:metabolism; D000818:Animals; D001237:Asphyxia / Q000378:metabolism; D001639:Bicarbonates / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002245:Carbon Dioxide / Q000378:metabolism*; D003051:Cochlea / Q000187:drug effects / Q000378:metabolism*; D004710:Endolymph / Q000187:drug effects / Q000378:metabolism*; D006168:Guinea Pigs; D006863:Hydrogen-Ion Concentration; D017736:Ion-Selective Electrodes; D008564:Membrane Potentials; D008839:Microelectrodes; D009543:Nifedipine / Q000494:pharmacology; D010477:Perfusion; D010498:Perilymph / Q000187:drug effects / Q000378:metabolism*; D013997:Time Factors
chemical_list: D001639:Bicarbonates; D002121:Calcium Channel Blockers; D000643:Ammonium Chloride; D002245:Carbon Dioxide; D009543:Nifedipine; D002118:Calcium