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Presence of type I and type II/IB receptors for adrenocorticosteroid hormones in the inner ear
1Department of Anatomy and Cell Biology, University of Florida College of Medicine, Gainesville 32610-0235.
Aldosterone-Type I and dexamethasone-Type II/IB receptor complexes were identified in cytosol prepared from both cochlear and vestibular tissue samples. The specific binding capacity of Type I receptors in the cochlear tissues was approximately equal to that in the vestibular tissues. Likewise, the binding capacity of Type II/IB receptors in the cochlea was approximately equal to that in the vestibular endorgans. Based on the total specific binding measured with dexamethasone, the Type II/IB receptors appeared to outnumber the Type I receptors in cochlear and vestibular tissues by a factor of approximately 2.6; however, when adjustments were made for the probable cross-binding of dexamethasone to Type I receptors, these ratios were decreased to approximately 1.6. The existence of protein receptors for adrenocorticosteroid hormones demonstrated in the present study clearly suggests a mechanism whereby such hormones may directly regulate fluid and ionic gradients in the inner ear.
Aldosterone-Type I and dexamethasone-Type II/IB receptor complexes were identified in cytosol prepared from both cochlear and vestibular tissue samples. The specific binding capacity of Type I receptors in the cochlear tissues was approximately equal to that in the vestibular tissues. Likewise, the binding capacity of Type II/IB receptors in the cochlea was approximately equal to that in the vestibular endorgans. Based on the total specific binding measured with dexamethasone, the Type II/IB receptors appeared to outnumber the Type I receptors in cochlear and vestibular tissues by a factor of approximately 2.6; however, when adjustments were made for the probable cross-binding of dexamethasone to Type I receptors, these ratios were decreased to approximately 1.6. The existence of protein receptors for adrenocorticosteroid hormones demonstrated in the present study clearly suggests a mechanism whereby such hormones may directly regulate fluid and ionic gradients in the inner ear.