| Autor: |
Pluteanu, Florentina, Heß, Johannes, Plackic, Jelena, Nikonova, Yulia, Preisenberger, Judit, Bukowska, Alicja, Schotten, Ulrich, Rinne, Andreas, Kienitz, Marie-Cecile, Schäfer, Martin K.-H., Weihe, Eberhard, Goette, Andreas, Kockskämper, Jens |
| Předmět: |
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| Zdroj: |
Cardiovascular Research; Apr2015, Vol. 106 Issue 1, p87-97, 11p |
| Abstrakt: |
Aims Hypertension is a major risk factor for atrial fibrillation.We hypothesized that arterial hypertension would alter atrial myocyte calcium (Ca2+) handling and that these alterations would serve to trigger atrial tachyarrhythmias. Methods and results Left atria or left atrial (LA)myocytes were isolated from spontaneously hypertensive rats (SHR) or normotensive Wistar-Kyoto (WKY) controls. Early after the onset of hypertension, at 3 months of age, there were no differences in Ca2+ transients (CaTs) or expression and phosphorylation of Ca2+ handling proteins between SHR and WKY. At 7 months of age, when left ventricular (LV) hypertrophy had progressed and markers of fibrosis were increased in left atrium, CaTs (at 1 Hz stimulation) were still unchanged. Subcellular alterations in Ca2+ handling were observed, however, in SHR atrial myocytes including (i) reduced expression of the a1C subunit of and reduced Ca2+ influx through L-type Ca2+ channels, (ii) reduced expression of ryanodine receptors with increased phosphorylation at Ser2808, (iii) decreased activity of the Na+/Ca2+ exchanger (at unaltered intracellular Na+ concentration), and (iv) increased SR Ca2+ load with reduced fractional release. These changes were associated with an increased propensity of SHR atrial myocytes to develop frequency-dependent, arrhythmogenic Ca2+ alternans. Conclusions In SHR, hypertension induces early subcellular LA myocyte Ca2+ remodelling during compensated LV hypertrophy. In basal conditions, atrial myocyte CaTs are not changed. At increased stimulation frequency, however, SHRatrial myocytes becomemoreprone to arrhythmogenic Ca2+ alternans, suggesting a link between hypertension, atrial Ca2+ homeostasis, and development of atrial tachyarrhythmias. [ABSTRACT FROM AUTHOR] |
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