February 4, 2008Proceedings of the National Academy of SciencesOpen Access

TASK channel deletion in mice causes primary hyperaldosteronism

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Why the study?

Does genetic deletion of TASK-1 and TASK-3 channels cause primary hyperaldosteronism in mice?

Population

Adult male mice with genetic deletion of TASK-1 and TASK-3 channels and age-matched wild-type controls.

Comparison

Genetic deletion of TASK-1 and TASK-3 channels vs Age-matched wild-type control mice

Design

Preclinical

Authors

LDLucinda A. DaviesUniversity of Leeds CHChanglong HuFuyang City People's Hospital NGNick A. GuagliardoUniversity of Virginia

Discussion

Member takes

Implication

Provides a murine model of nontumorigenic hyperaldosteronism; leaves open whether TASK modulation will translate to human therapy.

Structured PICO

Does genetic deletion of TASK-1 and TASK-3 channels cause primary hyperaldosteronism in mice?

Population

Adult male mice (mean age ~112-113 days) with genetic deletion of TASK-1 and TASK-3 channels (TASK-/-) and age-matched wild-type controls.

Intervention

Genetic deletion of TASK-1 and TASK-3 channels (TASK-/-)

Comparator

Age-matched wild-type control mice

Outcome

Aldosterone production and zona glomerulosa cell membrane potentialsurrogate

Genetic deletion of TASK-1 and TASK-3 channels in mice establishes an animal model of nontumorigenic primary hyperaldosteronism and identifies these channels as a potential therapeutic target.

Limitations

Use of conventional knockout mice cannot exclude contribution from other mechanisms of blood pressure control to the documented hypertension

Cite This Study

Davies et al. (2008) studied this question.

synapsesocial.com/papers/6a83647a0609b3655ee4e628 https://doi.org/10.1073/pnas.0712000105

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