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Cited by 198

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

TASK channel deletion in mice causes primary hyperaldosteronism

Open access
Davies, Lucinda A., Hu, Changlong, Guagliardo, Nick A., Sen, Neil, Chen, Xiangdong, Talley, Edmund M., Carey, Robert M., Bayliss, Douglas A., Barrett, Paula Q.·2008·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.0712000105
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Abstract

When inappropriate for salt status, the mineralocorticoid aldosterone induces cardiac and renal injury. Autonomous overproduction of aldosterone from the adrenal zona glomerulosa (ZG) is also the most frequent cause of secondary hypertension. Yet, the etiology of nontumorigenic primary hyperaldosteronism caused by bilateral idiopathic hyperaldosteronism remains unknown. Here, we show that genetic deletion of TWIK-related acid-sensitive K (TASK)-1 and TASK-3 channels removes an important background K current that results in a marked depolarization of ZG cell membrane potential. Although TASK channel deletion mice (TASK −/− ) adjust urinary Na excretion and aldosterone production to match Na intake, they produce more aldosterone than control mice across the range of Na intake. Overproduction of aldosterone is not the result of enhanced activity of the renin–angiotensin system because circulating renin concentrations remain either unchanged or lower than those of control mice at each level of Na intake. In addition, TASK −/− mice fail to suppress aldosterone production in response to dietary Na loading. Autonomous aldosterone production is also demonstrated by the failure of an angiotensin type 1 receptor blocker, candesartan, to normalize aldosterone production to control levels in TASK −/− mice. Thus, TASK −/− channel knockout mice exhibit the hallmarks of primary hyperaldosteronism. Our studies establish an animal model of nontumorigenic primary hyperaldosteronism and identify TASK channels as a possible therapeutic target for primary hyperaldosteronism.

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Metadata

Authors
Davies, L. A., Hu, C., Guagliardo, N. A., Sen, N., Chen, X., Talley, E. M., Carey, R. M., Bayliss, D. A., & Barrett, P. Q.
Venue
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Published
2008-02-12
Volume
105
Issue
6
Pages
2203-2208
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.0712000105
OpenAlex
W2163053410
Cited by
198
References
7
FWCI
9.15
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: TASK channel deletion in mice causes primary hyperaldosteronism. https://app.cochat.ai/papers/10.1073/pnas.0712000105
The paper
Davies, L. A., Hu, C., Guagliardo, N. A., Sen, N., Chen, X., Talley, E. M., Carey, R. M., Bayliss, D. A., & Barrett, P. Q. (2008). TASK channel deletion in mice causes primary hyperaldosteronism. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0712000105

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