Abstract
Mincralocorticoid excess syndromes are characterized by overactivity of amiloridesensitive sodium channels (ASSCs) in the distal tubule and collecting duct of the kidney, and presumably in other tissues. Most of the currently recognized, and widely accepted pathophysiological sequels of that overactivity can be explained by overactivity of the renal tubular ASSCs. However, sodium pumps are ubiquitous, and important effects of intrinsically overactive ASSCs or ASSCs activated by stimulated mineralocorticoid receptors (MRs) in other tissues, such as the brain and heart, are currently under investigation (1–4) and likely to be identified and clarified by future studies. Activation of MRs could also lead to important effects other than stimulation of ASSCs, but this is speculative.
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Gordon, R.D. (2001). Mineralocorticoid Excess Syndromes. In: Margioris, A.N., Chrousos, G.P. (eds) Adrenal Disorders. Contemporary Endocrinology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-101-5_27
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