Ventricular HCN channels decrease the repolarization reserve in the hypertrophic heart

Cardiovascular Research

Volumn 95, Issue 3, 2012, Pages 317-326

  Hofmann, Florian ^a   Fabritz, Larissa ^b,c   Stieber, Juliane ^a   Schmitt, Joachim ^d   Kirchhof, Paulus ^b,c   Ludwig, Andreas ^a   Herrmann, Stefan ^a  

^a UNIVERSITY HOSPITAL ERLANGEN   (Germany)

^b UNIVERSITY HOSPITAL MÜNSTER   (Germany)

^c UNIVERSITY OF BIRMINGHAM   (United Kingdom)

^d UNIVERSITY OF WÜRZBURG   (Germany)

Author keywords

Arrhythmia; HCN channels; Heart failure; Remodelling

Indexed keywords

CYCLIC NUCLEOTIDE GATED CHANNEL; HYPERPOLARIZATION ACTIVATED CYCLIC NUCLEOTIDE GATED CHANNEL 1; HYPERPOLARIZATION ACTIVATED CYCLIC NUCLEOTIDE GATED CHANNEL 2; HYPERPOLARIZATION ACTIVATED CYCLIC NUCLEOTIDE GATED CHANNEL 3; HYPERPOLARIZATION ACTIVATED CYCLIC NUCLEOTIDE GATED CHANNEL 4; UNCLASSIFIED DRUG; HCN2 POTASSIUM CHANNEL; HCN3 PROTEIN, MOUSE; HYPERPOLARIZATION ACTIVATED CATION CHANNEL; HYPERPOLARIZATION-ACTIVATED CATION CHANNEL; ION CHANNEL; MESSENGER RNA; POTASSIUM CHANNEL;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARRHYTHMOGENESIS; ARTICLE; CONTROLLED STUDY; GENE DELETION; HEART DEPOLARIZATION; HEART MUSCLE CELL; HEART MUSCLE POTENTIAL; HEART VENTRICLE HYPERTROPHY; MOUSE; NONHUMAN; PATHOPHYSIOLOGY; PRIORITY JOURNAL; PROTEIN EXPRESSION; QT PROLONGATION; UPREGULATION; ACTION POTENTIAL; ANIMAL; AORTA; C57BL MOUSE; DISEASE MODEL; ELECTROCARDIOGRAPHY; GENE EXPRESSION REGULATION; GENETICS; HEART ARRHYTHMIA; HEART LEFT VENTRICLE HYPERTROPHY; HEART VENTRICLE; HEART VENTRICLE REMODELING; LIGATION; METABOLISM; MOUSE MUTANT; PATHOLOGY; TIME;

ACTION POTENTIALS; ANIMALS; AORTA; ARRHYTHMIAS, CARDIAC; CYCLIC NUCLEOTIDE-GATED CATION CHANNELS; DISEASE MODELS, ANIMAL; ELECTROCARDIOGRAPHY; GENE EXPRESSION REGULATION; HEART VENTRICLES; HYPERTROPHY, LEFT VENTRICULAR; ION CHANNELS; LIGATION; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MYOCYTES, CARDIAC; POTASSIUM CHANNELS; RNA, MESSENGER; TIME FACTORS; VENTRICULAR REMODELING;

EID: 84865195928     PISSN: 00086363     EISSN: 17553245     Source Type: Journal    
DOI: 10.1093/cvr/cvs184     Document Type: Article

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