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REVIEW
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri
Submitted 7 July 2008 ; accepted in final form 27 February 2009
ABSTRACT
Pharmacological and physiological phenomena suggest that cells somewhere inside the central nervous system are responsive to aldosterone. Here, we present the fundamental physiological limitations for aldosterone action in the brain, including its limited blood-brain barrier penetration and its substantial competition from glucocorticoids. Recently, a small group of neurons with unusual sensitivity to circulating aldosterone were identified in the nucleus of the solitary tract. We review the discovery and characterization of these neurons, which express the enzyme 11β-hydroxysteroid dehydrogenase type 2, and consider alternative proposals regarding sites and mechanisms for mineralocorticoid action within the brain.
sodium deficiency; glucocorticoids; mineralocorticoids; nucleus of the solitary tract; blood-brain barrier; 11β-hydroxysteroid dehydrogenase
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