TASK channel deletion in mice causes primary hyperaldosteronism

Proceedings of the National Academy of Sciences of the United States of America

Volumn 105, Issue 6, 2008, Pages 2203-2208

  Davies, Lucinda A ^a   Hu, Changlong ^a   Guagliardo, Nick A ^a   Sen, Neil ^a   Chen, Xiangdong ^a   Talley, Edmund M ^a,b   Carey, Robert M ^a   Bayliss, Douglas A ^a   Barrett, Paula Q ^a  

^a UNIVERSITY OF VIRGINIA   (United States)

^b NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE   (United States)

Author keywords

Adrenal glomerulosa cells; Aldosterone; Potassium channels; Renin

Indexed keywords

ALDOSTERONE; CANDESARTAN; POTASSIUM CHANNEL; TWIK RELATED ACID SENSITIVE K 1 CHANNEL; TWIK RELATED ACID SENSITIVE K 3 CHANNEL; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; CELL MEMBRANE POTENTIAL; CONTROLLED STUDY; DEPOLARIZATION; GENE DELETION; MOUSE; NONHUMAN; POTASSIUM CURRENT; PRIMARY HYPERALDOSTERONISM; PRIORITY JOURNAL; RENIN ANGIOTENSIN ALDOSTERONE SYSTEM; SODIUM INTAKE; SODIUM URINE LEVEL;

ALDOSTERONE; ANIMALS; BASE SEQUENCE; DNA PRIMERS; HYPERALDOSTERONISM; IN SITU HYBRIDIZATION; MICE; MICE, KNOCKOUT; NERVE TISSUE PROTEINS; POTASSIUM CHANNELS, TANDEM PORE DOMAIN; RADIOIMMUNOASSAY;

ANIMALIA; MUS;

EID: 41149160175     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.0712000105     Document Type: Article

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