Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

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

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 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.

PMC Copyright notice

The mechanism thought to underlie hyperaldosteronism in patients with KCNJ5 mutations that cause Kir3.4 to lose its potassium selectivity. The mutated channels allow sodium entry, which triggers depolarization.

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; Ca_v 3.x, low-voltage activated calcium channels; Ca_v 1.x, high-voltage activated calcium channels; MC2R, ACTH receptor; ACTH, adrenocorticotropic hormone.