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. 2014 Apr 8;7:67–79. doi: 10.2147/TACG.S45620

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© 2014 Al-Salameh et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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The molecular mechanism thought to underlie hyperaldosteronism in patients with ATP1A1 mutations. The Na⁺/K⁺ ATPase changes from actively pumping (three Na⁺ outwards and two K⁺ inwards) to passive conduction of an inward current (protons or Na⁺ ions, depending on the mutation).

Abbreviations: CYP11B2, aldosterone synthase; TASK, TWIK-related acid sensitive K channels; Kir3.4, inwardly rectifying potassium channel Kir3.4; AT1R, type 1 angiotensin II receptor; H⁺, proton; Ca_v 3.x, low-voltage activated calcium channels; Ca_v 1.x, high-voltage activated calcium channels; MC2R, ACTH receptor; ACTH, adrenocorticotropic hormone.