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      The ubiquitous mineralocorticoid receptor: clinical implications.

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          Abstract

          Mineralocorticoid receptors (MR) exist in many tissues, in which they mediate diverse functions crucial to normal physiology, including tissue repair and electrolyte and fluid homeostasis. However, inappropriate activation of MR within these tissues, and especially in the brain, causes hypertension and pathological vascular, cardiac, and renal remodeling. MR binds aldosterone, cortisol and corticosterone with equal affinity. In aldosterone-target cells, co-expression with the 11β-hydroxysteroid dehydrogenase 2 (HSD2) allows aldosterone specifically to activate MR. Aldosterone levels are excessive in primary aldosteronism, but in conditions with increased oxidative stress, like CHF, obesity and diabetes, MR may also be inappropriately activated by glucocorticoids. Unlike thiazide diuretics, MR antagonists are diuretics that do not cause insulin resistance. Addition of MR antagonists to standard treatment for hypertension and cardiac or renal disease decreases end-organ pathology and sympathetic nerve activation (SNA), and increases quality of life indices.

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          Author and article information

          Journal
          Curr. Hypertens. Rep.
          Current hypertension reports
          1534-3111
          1522-6417
          Dec 2012
          : 14
          : 6
          Affiliations
          [1 ] G.V. Montgomery VA Medical Center, Jackson, MS 39216, USA. uhawkins@umc.edu
          Article
          NIHMS397159
          10.1007/s11906-012-0297-0
          3491176
          22843494

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