A negative correlation between endocochlear potential and endolymph potassium concentration

Abstract

It is widely accepted that the endocochlear potential (EP) arises from a secretion of K+ into endolymph by stria vascularis, although, as yet, there is no consensus concerning that cellular basis of this process. Studies in which changes in EP and endolymph potassium (Ke) were recorded during anoxia or treatment with transport inhibitors (e.g., ouabain) have shown that a decline of Ke is associated with the suppression of EP. On the basis of such experiments, it would be presumed that Ke would tend to be positively correlated with the magnitude of EP. On the contrary, a number of procedures have been found in which a decrease of Ke is associated with an increase of EP. Perilymphatic perfusion of solution containing 20 mM K+ caused a transient increase of EP (by up to 10 mV) followed by a decline. During this period, Ke recorded by ion‐selective microelectrodes typically showed a decrease, followed by an increase. Similarly, iontophoretic injection of Ca++ into endolymph produced an EP decrease that was mirrored by a Ke increase. These findings cannot be explained by changes in K+ transport and/or K+ permeability alone, but are more likely accounted for by changes in anion permeability. [Work supported by NIH Program Grant No. P01 NS24372.]