Antidiuretic hormone restores the endolymphatic longitudinal K+ gradient in the Brattleboro rat cochlea.

In the cochlea, endolymph is hyperosmotic to plasma and perilymph. To test the hypothesis that antidiuretic hormone is involved in the modulation of endolymph secretion, the electrochemical composition of cochlear fluids, endolymph and perilymph, was studied in three groups of anaesthetized rats: control Long Evans rats, homozygous Brattleboro rats that are genetically deprived of antidiuretic hormone, and Brattleboro rats that were treated with antidiuretic hormone (dDAVP, 0.5 microgram/100 g body weight/24 h during 8 days). Endolymph was sampled from the scala media at each turn of the cochlea and perilymph from the scala vestibuli. In Long Evans rats, the endocochlear potential, the endolymphatic K+ and Cl- concentrations decreased from base to apex of the cochlea as previously reported in guinea pigs and Sprague Dawley rats. In Brattleboro rats, the endocochlear potential and the Cl- concentration gradients were still present, whereas the K+ concentration gradient were still present, whereas the K+ concentration gradient was absent. This K+ gradient was restored by the administration of dDAVP, which increased the K+ concentration at the base of the cochlea. This work indicates that the K+ secretion in endolymph, and thus the osmolality, may be locally modulated by the antidiuretic hormone, probably via V2 receptors.