Am J Physiol Cell Physiol AJP: Regulatory, Integrative and Comparative Physiology
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Am J Physiol Cell Physiol 283: C1752-C1760, 2002. First published August 28, 2002; doi:10.1152/ajpcell.00283.2002
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Vol. 283, Issue 6, C1752-C1760, December 2002

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

Pierre G. Milhaud1, Satyanarayana R. Pondugula2, Jun Ho Lee2, Michael Herzog2, Jacques Lehouelleur1, Philine Wangemann2, Alain Sans1, and Daniel C. Marcus2

1 Institut National de la Santé et de la Recherche Médicale Unité 432 Vestibular Neurobiology, Université Montpellier II, 34095 Montpellier, France; and 2 Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506

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 (Isc) 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 Isc 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 Isc. Isoproterenol stimulation of Isc and cAMP was inhibited by ICI-118551 (IC50 = 6 µM for Isc) but not by CGP-20712A (1 µM) in primary cultures, and similar results were found in native epithelium. Isc 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.

anion secretion; vestibular labyrinth; receptors; endolymph


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