Increased β-adrenergic inotropy in ventricular myocardium from Trpm4−/− mice
Rationale:The Trpm4 gene has recently been associated with several disorders, including cardiac conduction diseases and Brugada syndrome. Transient receptor potential member 4 (TRPM4) proteins constitute Ca2+-activated, but Ca2+-impermeable, nonselective cation channels and are expressed both in atr...
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| Main Authors: | , , , , , , , , , , , |
|---|---|
| Format: | Article (Journal) |
| Language: | English |
| Published: |
2014
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| In: |
Circulation research
Year: 2013, Volume: 114, Issue: 2, Pages: 283-294 |
| ISSN: | 1524-4571 |
| DOI: | 10.1161/CIRCRESAHA.114.302835 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1161/CIRCRESAHA.114.302835 Verlag, lizenzpflichtig, Volltext: https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.114.302835 
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| Author Notes: | Mathar Ilka, Kecskes Miklos, Van der Mieren Gerry, Jacobs Griet, Camacho Londoño Juan E., Uhl Sebastian, Flockerzi Veit, Voets Thomas, Freichel Marc, Nilius Bernd, Herijgers Paul, Vennekens Rudi |
MARC
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| 245 | 1 | 0 | |a Increased β-adrenergic inotropy in ventricular myocardium from Trpm4−/− mice |c Mathar Ilka, Kecskes Miklos, Van der Mieren Gerry, Jacobs Griet, Camacho Londoño Juan E., Uhl Sebastian, Flockerzi Veit, Voets Thomas, Freichel Marc, Nilius Bernd, Herijgers Paul, Vennekens Rudi |
| 246 | 3 | 0 | |a minus four |
| 246 | 3 | 3 | |a Increased beta-adrenergic inotropy in ventricular myocardium from Trpm four minus slash minus mice |
| 246 | 3 | 3 | |a Increased beta-adrenergic inotropy in ventricular myocardium from Trpm4 −/− mice |
| 264 | 1 | |c 2014 | |
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| 520 | |a Rationale:The Trpm4 gene has recently been associated with several disorders, including cardiac conduction diseases and Brugada syndrome. Transient receptor potential member 4 (TRPM4) proteins constitute Ca2+-activated, but Ca2+-impermeable, nonselective cation channels and are expressed both in atrial and in ventricular cardiomyocytes. The physiological function of TRPM4 in the heart remains, however, incompletely understood.Objective:To establish the role of TRPM4 in cardiac muscle function.Methods and Results:We used TRPM4 knockout mice and performed patch-clamp experiments, membrane potential measurements, microfluorometry, contractility measurements, and in vivo pressure-volume loop analysis. We demonstrate that TRPM4 proteins are functionally present in mouse ventricular myocytes and are activated on Ca2+-induced Ca2+ release. In Trpm4−/− mice, cardiac muscle displays an increased β-adrenergic inotropic response both in vitro and in vivo. Measurements of action potential duration show a significantly decreased time for 50% and 90% repolarization in Trpm4−/− ventricular myocytes. We provide evidence that this change in action potential shape leads to an increased driving force for the L-type Ca2+ current during the action potential, which explains the altered contractility of the heart muscle.Conclusions:Our results show that functional TRPM4 proteins are novel determinants of the inotropic effect of β-adrenergic stimulation on the ventricular heart muscle. | ||
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| 700 | 1 | |a Van der Mieren, Gerry |e VerfasserIn |4 aut | |
| 700 | 1 | |a Jacobs, Griet |e VerfasserIn |4 aut | |
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| 700 | 1 | |a Herijgers, Paul |e VerfasserIn |4 aut | |
| 700 | 1 | |a Vennekens, Rudi |e VerfasserIn |4 aut | |
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