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Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers
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| Zeitschriftentitel: | European Journal of Heart Failure |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , |
| In: | European Journal of Heart Failure, 10, 2008, 5, S. 439-445 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Lorenz, Mario Hellige, Niels Rieder, Philipp Kinkel, Hans‐Tilmann Trimpert, Christiane Staudt, Alexander Felix, Stephan B. Baumann, Gert Stangl, Karl Stangl, Verena Lorenz, Mario Hellige, Niels Rieder, Philipp Kinkel, Hans‐Tilmann Trimpert, Christiane Staudt, Alexander Felix, Stephan B. Baumann, Gert Stangl, Karl Stangl, Verena |
|---|---|
| author |
Lorenz, Mario Hellige, Niels Rieder, Philipp Kinkel, Hans‐Tilmann Trimpert, Christiane Staudt, Alexander Felix, Stephan B. Baumann, Gert Stangl, Karl Stangl, Verena |
| spellingShingle |
Lorenz, Mario Hellige, Niels Rieder, Philipp Kinkel, Hans‐Tilmann Trimpert, Christiane Staudt, Alexander Felix, Stephan B. Baumann, Gert Stangl, Karl Stangl, Verena European Journal of Heart Failure Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers Cardiology and Cardiovascular Medicine |
| author_sort |
lorenz, mario |
| spelling |
Lorenz, Mario Hellige, Niels Rieder, Philipp Kinkel, Hans‐Tilmann Trimpert, Christiane Staudt, Alexander Felix, Stephan B. Baumann, Gert Stangl, Karl Stangl, Verena 1388-9842 1879-0844 Wiley Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1016/j.ejheart.2008.03.004 <jats:title>Abstract</jats:title><jats:sec><jats:title>Background:</jats:title><jats:p>There is evidence that the tea catechin epigallocatechin‐3‐gallate (EGCG) modulates myocardial contractility. However, the underlying mechanisms remain to be determined.</jats:p></jats:sec><jats:sec><jats:title>Aims:</jats:title><jats:p>To study potential signalling pathways involved in EGCG‐induced contractile parameters.</jats:p></jats:sec><jats:sec><jats:title>Methods and results:</jats:title><jats:p>EGCG increased fractional shortening in rat cardiac myocytes and enhanced intracellular systolic Ca<jats:sup>2+</jats:sup> concentrations. In isolated rat hearts, perfusion with EGCG resulted in significant, dose‐dependent increase in peak systolic left ventricular pressure, as well as in contraction and relaxation velocities. Heart rate did not change. Inhibition of the β<jats:sub>1</jats:sub>‐receptor with metoprolol had no influence on the contractile effects of EGCG. Furthermore, levels of cAMP and phosphorylation of phospholamban did not change with EGCG, indicating that the beta‐receptor pathway is not involved. The L‐type Ca<jats:sup>2+</jats:sup> channel inhibitors, nifedipine and gallopamil, failed to modulate EGCG‐induced increase in contractility. However, the myocardial effects and intracellular calcium transients stimulated by EGCG were significantly reduced by the antagonist of the Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger (NHE) methyl‐<jats:italic>N</jats:italic>‐isobutyl amiloride (MIA), and by blocking of the reverse mode of the Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> exchanger (NCX) by KB‐R7943.</jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p>These results indicate that Ca<jats:sup>2+</jats:sup>‐dependent positive inotropic and lusitropic effects of EGCG are mediated in part via activation of the Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger and the reverse mode of the Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> exchanger in the rat myocardium.</jats:p></jats:sec> Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na<sup>+</sup>/H<sup>+</sup> and Na<sup>+</sup>/Ca<sup>2+</sup> exchangers European Journal of Heart Failure |
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10.1016/j.ejheart.2008.03.004 |
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Medizin |
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Wiley, 2008 |
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Wiley, 2008 |
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1388-9842 1879-0844 |
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lorenz2008positiveinotropiceffectsofepigallocatechin3gallateegcginvolveactivationofnahandnaca2exchangers |
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2008 |
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Wiley |
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European Journal of Heart Failure |
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49 |
| title |
Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_unstemmed |
Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_full |
Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_fullStr |
Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_full_unstemmed |
Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_short |
Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_sort |
positive inotropic effects of epigallocatechin‐3‐gallate (egcg) involve activation of na<sup>+</sup>/h<sup>+</sup> and na<sup>+</sup>/ca<sup>2+</sup> exchangers |
| topic |
Cardiology and Cardiovascular Medicine |
| url |
http://dx.doi.org/10.1016/j.ejheart.2008.03.004 |
| publishDate |
2008 |
| physical |
439-445 |
| description |
<jats:title>Abstract</jats:title><jats:sec><jats:title>Background:</jats:title><jats:p>There is evidence that the tea catechin epigallocatechin‐3‐gallate (EGCG) modulates myocardial contractility. However, the underlying mechanisms remain to be determined.</jats:p></jats:sec><jats:sec><jats:title>Aims:</jats:title><jats:p>To study potential signalling pathways involved in EGCG‐induced contractile parameters.</jats:p></jats:sec><jats:sec><jats:title>Methods and results:</jats:title><jats:p>EGCG increased fractional shortening in rat cardiac myocytes and enhanced intracellular systolic Ca<jats:sup>2+</jats:sup> concentrations. In isolated rat hearts, perfusion with EGCG resulted in significant, dose‐dependent increase in peak systolic left ventricular pressure, as well as in contraction and relaxation velocities. Heart rate did not change. Inhibition of the β<jats:sub>1</jats:sub>‐receptor with metoprolol had no influence on the contractile effects of EGCG. Furthermore, levels of cAMP and phosphorylation of phospholamban did not change with EGCG, indicating that the beta‐receptor pathway is not involved. The L‐type Ca<jats:sup>2+</jats:sup> channel inhibitors, nifedipine and gallopamil, failed to modulate EGCG‐induced increase in contractility. However, the myocardial effects and intracellular calcium transients stimulated by EGCG were significantly reduced by the antagonist of the Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger (NHE) methyl‐<jats:italic>N</jats:italic>‐isobutyl amiloride (MIA), and by blocking of the reverse mode of the Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> exchanger (NCX) by KB‐R7943.</jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p>These results indicate that Ca<jats:sup>2+</jats:sup>‐dependent positive inotropic and lusitropic effects of EGCG are mediated in part via activation of the Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger and the reverse mode of the Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> exchanger in the rat myocardium.</jats:p></jats:sec> |
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| author | Lorenz, Mario, Hellige, Niels, Rieder, Philipp, Kinkel, Hans‐Tilmann, Trimpert, Christiane, Staudt, Alexander, Felix, Stephan B., Baumann, Gert, Stangl, Karl, Stangl, Verena |
| author_facet | Lorenz, Mario, Hellige, Niels, Rieder, Philipp, Kinkel, Hans‐Tilmann, Trimpert, Christiane, Staudt, Alexander, Felix, Stephan B., Baumann, Gert, Stangl, Karl, Stangl, Verena, Lorenz, Mario, Hellige, Niels, Rieder, Philipp, Kinkel, Hans‐Tilmann, Trimpert, Christiane, Staudt, Alexander, Felix, Stephan B., Baumann, Gert, Stangl, Karl, Stangl, Verena |
| author_sort | lorenz, mario |
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| description | <jats:title>Abstract</jats:title><jats:sec><jats:title>Background:</jats:title><jats:p>There is evidence that the tea catechin epigallocatechin‐3‐gallate (EGCG) modulates myocardial contractility. However, the underlying mechanisms remain to be determined.</jats:p></jats:sec><jats:sec><jats:title>Aims:</jats:title><jats:p>To study potential signalling pathways involved in EGCG‐induced contractile parameters.</jats:p></jats:sec><jats:sec><jats:title>Methods and results:</jats:title><jats:p>EGCG increased fractional shortening in rat cardiac myocytes and enhanced intracellular systolic Ca<jats:sup>2+</jats:sup> concentrations. In isolated rat hearts, perfusion with EGCG resulted in significant, dose‐dependent increase in peak systolic left ventricular pressure, as well as in contraction and relaxation velocities. Heart rate did not change. Inhibition of the β<jats:sub>1</jats:sub>‐receptor with metoprolol had no influence on the contractile effects of EGCG. Furthermore, levels of cAMP and phosphorylation of phospholamban did not change with EGCG, indicating that the beta‐receptor pathway is not involved. The L‐type Ca<jats:sup>2+</jats:sup> channel inhibitors, nifedipine and gallopamil, failed to modulate EGCG‐induced increase in contractility. However, the myocardial effects and intracellular calcium transients stimulated by EGCG were significantly reduced by the antagonist of the Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger (NHE) methyl‐<jats:italic>N</jats:italic>‐isobutyl amiloride (MIA), and by blocking of the reverse mode of the Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> exchanger (NCX) by KB‐R7943.</jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p>These results indicate that Ca<jats:sup>2+</jats:sup>‐dependent positive inotropic and lusitropic effects of EGCG are mediated in part via activation of the Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger and the reverse mode of the Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> exchanger in the rat myocardium.</jats:p></jats:sec> |
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| spelling | Lorenz, Mario Hellige, Niels Rieder, Philipp Kinkel, Hans‐Tilmann Trimpert, Christiane Staudt, Alexander Felix, Stephan B. Baumann, Gert Stangl, Karl Stangl, Verena 1388-9842 1879-0844 Wiley Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1016/j.ejheart.2008.03.004 <jats:title>Abstract</jats:title><jats:sec><jats:title>Background:</jats:title><jats:p>There is evidence that the tea catechin epigallocatechin‐3‐gallate (EGCG) modulates myocardial contractility. However, the underlying mechanisms remain to be determined.</jats:p></jats:sec><jats:sec><jats:title>Aims:</jats:title><jats:p>To study potential signalling pathways involved in EGCG‐induced contractile parameters.</jats:p></jats:sec><jats:sec><jats:title>Methods and results:</jats:title><jats:p>EGCG increased fractional shortening in rat cardiac myocytes and enhanced intracellular systolic Ca<jats:sup>2+</jats:sup> concentrations. In isolated rat hearts, perfusion with EGCG resulted in significant, dose‐dependent increase in peak systolic left ventricular pressure, as well as in contraction and relaxation velocities. Heart rate did not change. Inhibition of the β<jats:sub>1</jats:sub>‐receptor with metoprolol had no influence on the contractile effects of EGCG. Furthermore, levels of cAMP and phosphorylation of phospholamban did not change with EGCG, indicating that the beta‐receptor pathway is not involved. The L‐type Ca<jats:sup>2+</jats:sup> channel inhibitors, nifedipine and gallopamil, failed to modulate EGCG‐induced increase in contractility. However, the myocardial effects and intracellular calcium transients stimulated by EGCG were significantly reduced by the antagonist of the Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger (NHE) methyl‐<jats:italic>N</jats:italic>‐isobutyl amiloride (MIA), and by blocking of the reverse mode of the Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> exchanger (NCX) by KB‐R7943.</jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p>These results indicate that Ca<jats:sup>2+</jats:sup>‐dependent positive inotropic and lusitropic effects of EGCG are mediated in part via activation of the Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger and the reverse mode of the Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> exchanger in the rat myocardium.</jats:p></jats:sec> Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na<sup>+</sup>/H<sup>+</sup> and Na<sup>+</sup>/Ca<sup>2+</sup> exchangers European Journal of Heart Failure |
| spellingShingle | Lorenz, Mario, Hellige, Niels, Rieder, Philipp, Kinkel, Hans‐Tilmann, Trimpert, Christiane, Staudt, Alexander, Felix, Stephan B., Baumann, Gert, Stangl, Karl, Stangl, Verena, European Journal of Heart Failure, Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers, Cardiology and Cardiovascular Medicine |
| title | Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_full | Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_fullStr | Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_full_unstemmed | Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_short | Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| title_sort | positive inotropic effects of epigallocatechin‐3‐gallate (egcg) involve activation of na<sup>+</sup>/h<sup>+</sup> and na<sup>+</sup>/ca<sup>2+</sup> exchangers |
| title_unstemmed | Positive inotropic effects of epigallocatechin‐3‐gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers |
| topic | Cardiology and Cardiovascular Medicine |
| url | http://dx.doi.org/10.1016/j.ejheart.2008.03.004 |