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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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Regulation of aldosterone secretion in the physiologic state. Binding of angiotensin II to the AT1R blocks Kir3.4 potassium channels, TASK and Na⁺/K⁺ ATPase (1), this depolarizes the membrane (2) and results in the opening of voltage-gated Ca²⁺ channels (3). The resulting increase in intracellular levels provides the signal for increased expression of aldosterone synthase (4) through many different actions (including increased transcription of steroidogenic acute regulator protein).

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; ATII, angiotensin II; Ca_v 3.x, low-voltage activated calcium channels; Ca_v 1.x, high-voltage activated calcium channels; MC2R, ACTH receptor; ACTH, adrenocorticotropic hormone; StAR, steroidogenic acute regulator protein.