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Articles in PresS, published online ahead of print August 28, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00283.2002
Submitted on June 20, 2002
Accepted on August 19, 2002
1 INSERM U432 Vestibular Neurobiology, Universite Montpellier II, Montpellier, France
2 Anatomy & Physiology, Kansas State University, Manhattan, KS, USA
* To whom correspondence should be addressed. E-mail: marcus{at}ksu.edu.
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 (10 µM). Isoproterenol and norepinephrine increased Isc with an EC50 of 3 nM and 15 nM, respectively, and isoproterenol increased tissue cAMP (native canals) with an EC50 of 5 nM. There was no further increase in Isc by addition of forskolin after maximal stimulation by isoproterenol. Agonists for adenosine, histamine and vasopressin receptors had no effect on Isc. Isoproterenol stimulation of Isc and cAMP was inhibited by ICI118551 (IC50 6 µM for Isc) but not by CGP20712A (1 µM) in primary cultures and similar results found in native epithelium. Isc was partially inhibited by basolateral Ba2+ (IC50 0.27 mM) and ouabain while 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 ß2-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.
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