Overview

K⁺≈150 mmol/L

Na⁺≈1 mmol/L

Endocochlear potential≈+80 mV

Endolymph is unique among extracellular fluids in having an intracellular-like composition: K⁺ ≈150 mmol/L, Na⁺ ≈1 mmol/L, very low Ca²⁺ (≈20–30 µmol/L) and high Cl⁻. It fills the cochlear duct, utricle, saccule, semicircular ducts and endolymphatic duct and sac.

In the cochlea it is secreted by the stria vascularis on the lateral wall of the cochlear duct: K⁺ is recycled from hair cells via supporting cells and fibrocytes (connected by gap junctions containing connexin 26) and pumped into endolymph by marginal cells (Na⁺/K⁺-ATPase, NKCC1, KCNQ1/KCNE1 channels). This generates the endocochlear potential (EP) of ≈+80 mV relative to perilymph. With hair-cell interiors at ≈−45 to −70 mV, the driving force for K⁺ entry through the transduction channels is ≈125–150 mV — the largest in the body — which makes hair cells exceptionally sensitive and fast. In the vestibular system endolymph is secreted by vestibular dark cells and has a near-zero potential.

Endolymph flows slowly (longitudinal flow) towards the endolymphatic sac, where it is resorbed. Its inertia relative to the canal walls is what deflects the cupula in the semicircular canals.

Location: Membranous labyrinth: cochlear duct (scala media), utricle, saccule, semicircular ducts, endolymphatic duct and sac.

Function

Provide K⁺ for hair-cell mechanotransduction
Create the endocochlear potential that amplifies the transduction current
Its inertia transduces angular acceleration in the semicircular ducts

Physiology: Composition (approx.): K⁺ 150, Na⁺ 1, Cl⁻ 130 mmol/L, Ca²⁺ 0.02–0.03 mmol/L; EP ≈+80 mV (scala media). Loop diuretics (furosemide) inhibit NKCC1 in the stria vascularis, lowering the EP — hence their ototoxicity.
Secretions: Produced by the stria vascularis (cochlea) and vestibular dark cells; absorbed in the endolymphatic sac.

Clinical significance

Ménière disease (endolymphatic hydrops)

Excess endolymph distends the membranous labyrinth. Classic tetrad: episodic vertigo lasting 20 min–12 h, fluctuating low-frequency sensorineural hearing loss, tinnitus and aural fullness; usually unilateral, middle age. Hearing deteriorates progressively; Tumarkin drop attacks (otolithic crises) may occur. Management: low-salt diet, betahistine, diuretics, intratympanic steroids or gentamicin, surgery.

Connexin 26 (GJB2) deafness

Mutations in GJB2, which encodes the gap-junction protein connexin 26 needed for K⁺ recycling to the stria vascularis, are the most common cause of congenital non-syndromic sensorineural hearing loss.

Jervell and Lange-Nielsen syndrome

Recessive mutations in KCNQ1/KCNE1 — K⁺ channels used both by strial marginal cells and cardiac myocytes — cause congenital deafness with long QT syndrome (risk of sudden death).

Test yourself

Which of the following correctly describes endolymph?

High Na⁺, low K⁺, resembles CSF
Fills the scala vestibuli and scala tympani
High K⁺, low Na⁺, secreted by the stria vascularis
Drains through the cochlear aqueduct into the subarachnoid space

Answer: High K⁺, low Na⁺, secreted by the stria vascularis

Endolymph (K⁺ ≈150, Na⁺ ≈1 mmol/L) fills the membranous labyrinth including the scala media; the stria vascularis secretes it and generates the +80 mV endocochlear potential. Perilymph (high Na⁺) fills the scala vestibuli and tympani and communicates with CSF.