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Chloride secretion by semicircular canal duct epithelium is stimulated via beta 2-adrenergic receptors.

The ductal epithelium of the semicircular canal forms much of the boundary between the K+-rich luminal fluid and the Na+-rich abluminal fluid. We sought to determine whether the net ion flux producing the apical-to-basal short-circuit current (I(sc)) in primary cultures was due to anion secretion and/or cation absorption and under control of receptor agonists. Net fluxes of 22Na, 86Rb, and 36Cl demonstrated a basal-to-apical Cl- secretion that was stimulated by isoproterenol. Isoproterenol and norepinephrine increased I(sc) with an EC50 of 3 and 15 nM, respectively, and isoproterenol increased tissue cAMP of native canals with an EC50 of 5 nM. Agonists for adenosine, histamine, and vasopressin receptors had no effect on I(sc). Isoproterenol stimulation of I(sc) and cAMP was inhibited by ICI-118551 (IC50 = 6 microM for I(sc)) but not by CGP-20712A (1 microM) in primary cultures, and similar results were found in native epithelium. I(sc) was partially inhibited by basolateral Ba2+ (IC50 = 0.27 mM) and ouabain, whereas responses to genistein, glibenclamide, and DIDS did not fully fit the profile for CFTR. Our findings show that the canal epithelium contributes to endolymph homeostasis by secretion of Cl- under beta 2 adrenergic control with cAMP as second messenger, a process that parallels the adrenergic control of K+ secretion by vestibular dark cells. The current work points to one possible etiology of endolymphatic hydrops in Meniere's disease and may provide a basis for intervention.