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Diminished Kv4.2/3 but not KChIP2 levels reduce the cardiac transient outward K+ current in spontaneously hypertensive rats.

Standard

Diminished Kv4.2/3 but not KChIP2 levels reduce the cardiac transient outward K+ current in spontaneously hypertensive rats. / Goltz, Diane; Schultz, Jobst-Hendrik; Stucke, Carolin; Wagner, Michael E.; Bassalaý, Peter; Schwoerer, Alexander; Ehmke, Heimo; Volk, Tilmann.

in: CARDIOVASC RES, Jahrgang 74, Nr. 1, 1, 2007, S. 85-95.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Goltz, D, Schultz, J-H, Stucke, C, Wagner, ME, Bassalaý, P, Schwoerer, A, Ehmke, H & Volk, T 2007, 'Diminished Kv4.2/3 but not KChIP2 levels reduce the cardiac transient outward K+ current in spontaneously hypertensive rats.', CARDIOVASC RES, Jg. 74, Nr. 1, 1, S. 85-95. <http://www.ncbi.nlm.nih.gov/pubmed/17289007?dopt=Citation>

APA

Goltz, D., Schultz, J-H., Stucke, C., Wagner, M. E., Bassalaý, P., Schwoerer, A., Ehmke, H., & Volk, T. (2007). Diminished Kv4.2/3 but not KChIP2 levels reduce the cardiac transient outward K+ current in spontaneously hypertensive rats. CARDIOVASC RES, 74(1), 85-95. [1]. http://www.ncbi.nlm.nih.gov/pubmed/17289007?dopt=Citation

Vancouver

Goltz D, Schultz J-H, Stucke C, Wagner ME, Bassalaý P, Schwoerer A et al. Diminished Kv4.2/3 but not KChIP2 levels reduce the cardiac transient outward K+ current in spontaneously hypertensive rats. CARDIOVASC RES. 2007;74(1):85-95. 1.

Bibtex

@article{f382a99daa624b0da9b0d98b48b679a6,
title = "Diminished Kv4.2/3 but not KChIP2 levels reduce the cardiac transient outward K+ current in spontaneously hypertensive rats.",
abstract = "OBJECTIVE: A reduction of the Ca(2+)-independent transient outward potassium current (I(to)) in epicardial but not in endocardial myocytes of the left ventricle has been observed in cardiac hypertrophy and is thought to contribute to the electrical vulnerability associated with this pathology. METHODS: In the present study we investigated the molecular mechanisms underlying regional alterations in I(to) in hypertrophied hearts of spontaneously hypertensive rats (SHR) using the whole-cell patch-clamp technique, quantitative RT-PCR and heterologous expression of underlying ion channel subunits. RESULTS: I(to) was significantly smaller in epicardial myocytes of SHR than in Wistar-Kyoto (WKY) controls (11.1+/-0.9 pA/pF, n=20 vs. 16.8+/-1.7 pA/pF, n=20, p",
author = "Diane Goltz and Jobst-Hendrik Schultz and Carolin Stucke and Wagner, {Michael E.} and Peter Bassala{\'y} and Alexander Schwoerer and Heimo Ehmke and Tilmann Volk",
year = "2007",
language = "Deutsch",
volume = "74",
pages = "85--95",
journal = "CARDIOVASC RES",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "1",

}

RIS

TY - JOUR

T1 - Diminished Kv4.2/3 but not KChIP2 levels reduce the cardiac transient outward K+ current in spontaneously hypertensive rats.

AU - Goltz, Diane

AU - Schultz, Jobst-Hendrik

AU - Stucke, Carolin

AU - Wagner, Michael E.

AU - Bassalaý, Peter

AU - Schwoerer, Alexander

AU - Ehmke, Heimo

AU - Volk, Tilmann

PY - 2007

Y1 - 2007

N2 - OBJECTIVE: A reduction of the Ca(2+)-independent transient outward potassium current (I(to)) in epicardial but not in endocardial myocytes of the left ventricle has been observed in cardiac hypertrophy and is thought to contribute to the electrical vulnerability associated with this pathology. METHODS: In the present study we investigated the molecular mechanisms underlying regional alterations in I(to) in hypertrophied hearts of spontaneously hypertensive rats (SHR) using the whole-cell patch-clamp technique, quantitative RT-PCR and heterologous expression of underlying ion channel subunits. RESULTS: I(to) was significantly smaller in epicardial myocytes of SHR than in Wistar-Kyoto (WKY) controls (11.1+/-0.9 pA/pF, n=20 vs. 16.8+/-1.7 pA/pF, n=20, p

AB - OBJECTIVE: A reduction of the Ca(2+)-independent transient outward potassium current (I(to)) in epicardial but not in endocardial myocytes of the left ventricle has been observed in cardiac hypertrophy and is thought to contribute to the electrical vulnerability associated with this pathology. METHODS: In the present study we investigated the molecular mechanisms underlying regional alterations in I(to) in hypertrophied hearts of spontaneously hypertensive rats (SHR) using the whole-cell patch-clamp technique, quantitative RT-PCR and heterologous expression of underlying ion channel subunits. RESULTS: I(to) was significantly smaller in epicardial myocytes of SHR than in Wistar-Kyoto (WKY) controls (11.1+/-0.9 pA/pF, n=20 vs. 16.8+/-1.7 pA/pF, n=20, p

M3 - SCORING: Zeitschriftenaufsatz

VL - 74

SP - 85

EP - 95

JO - CARDIOVASC RES

JF - CARDIOVASC RES

SN - 0008-6363

IS - 1

M1 - 1

ER -