Potassium currents in vestibular type II hair cells activated by hydrostatic pressure.

An elevated hydrostatic pressure in the endolymphatic space of the inner ear is discussed as pathophysiological factor in hydrops-related diseases of the inner ear. An increase in pressure by fractions of 1 cm H(2)O is sufficient to induce vertigo-like symptoms in animal models. To establish a link between hydrostatic pressure and the function of vestibular hair cells, we studied potassium currents in isolated vestibular type II hair cells from guinea-pig utricles when the hydrostatic pressure was increased by raising the height of the bath from 0.2-0.5, 0.7 or 1.0 cm. Elevated pressure enhanced K(+) currents significantly; a rise in pressure from 0.2-0.5 cm H(2)O increased the total K(+) current at +40 mV by 22+/-14% (+/-S.D.). The pressure-sensitive current I(K,p) was non-inactivating during depolarizing pulses. It was maintained when the pressure was kept elevated for several minutes and receded promptly after return to a pressure of 0.2 cm H(2)O. Voltage-gated Ca(2+) currents, in contrast, were not altered by hydrostatic pressure. A pharmacological characterization of I(K,p) revealed that tetraetylammonium (100 mM) abolished all outward currents including I(K,p). I(K,p) was partly and reversibly inhibited by 4-aminopyridine. Dihydrostreptomycin, a blocker of the transduction channel, left I(K,p) unaffected. Charybdotoxin (100 nM), a blocker of Ca(2+)-dependent K(+) channels, completely yet reversibly abolished I(K,p). We conclude that small elevations in hydrostatic pressure evoke a charybdotoxin-sensitive, probably Ca(2+)-dependent K(+) current in vestibular hair cells. This is likely to alter their frequency response and may be a relevant mechanism how hydrostatic pressure disturbs transduction.