Kir6.2-deficient mice are susceptible to stimulated ANP secretion: K ATP channel acts as a negative feedback mechanism?

Cardiovascular Research

Volumn 67, Issue 1, 2005, Pages 60-68

  Saegusa, Noriko ^a   Sato, Toshiaki ^a   Saito, Tomoaki ^a   Tamagawa, Masaji ^a   Komuro, Issei ^a   Nakaya, Haruaki ^a  

^a CHIBA UNIVERSITY   (Japan)

Author keywords

K ATP channel; Myocytes; Natriuretic peptide

Indexed keywords

2,4 DINITROPHENOL; ADENOSINE TRIPHOSPHATE; ATRIAL NATRIURETIC FACTOR; GLIBENCLAMIDE; INWARDLY RECTIFYING POTASSIUM CHANNEL SUBUNIT KIR6.2;

ANESTHESIA; ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BATH; CELL ISOLATION; CELL STIMULATION; CONTROLLED STUDY; EXPOSURE; FEEDBACK SYSTEM; HEART ATRIUM; HEART MUSCLE CELL; HEART VOLUME; HOMOZYGOSITY; HYPOTENSION; ION CURRENT; ISOLATED HEART; KNOCKOUT GENE; MODULATION; MOLECULAR MECHANICS; MOUSE; MUSCLE HYPOTONIA; MUSCLE STRETCHING; NONHUMAN; PATCH CLAMP; PRIORITY JOURNAL; PROTEIN ANALYSIS; PROTEIN BLOOD LEVEL; PROTEIN CONTENT; PROTEIN INDUCTION; PROTEIN SECRETION; RADIOIMMUNOASSAY; RECORDING; SENSITIVITY ANALYSIS; SINUS NODE MEMBRANE POTENTIAL; WILD TYPE;

ACTION POTENTIALS; ANIMALS; AORTA; ATRIAL NATRIURETIC FACTOR; CELLS, CULTURED; FEEDBACK, BIOCHEMICAL; HEART ATRIA; MICE; MICE, KNOCKOUT; MYOCYTES, CARDIAC; PATCH-CLAMP TECHNIQUES; POTASSIUM CHANNELS; POTASSIUM CHANNELS, INWARDLY RECTIFYING; STIMULATION, CHEMICAL;

EID: 20444424162     PISSN: 00086363     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.cardiores.2005.03.011     Document Type: Article

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