Atrial tachyarrhythmia in Rgs5-null mice.
Atrial tachyarrhythmia in Rgs5-null mice.
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Rgs5 缺失小鼠的房性快速心律失常
DOI:
10.1371/journal.pone.0046856
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Huang C
中科院分区:
文献类型:
--
作者:
Qin M;Huang H;Wang T;Hu H;Liu Y;Gu Y;Cao H;Li H;Huang C
Aims The aim of this study was to elucidate the effects of regulator of G-protein signaling 5 (Rgs5), a negative regulator of G protein-mediated signaling, on atrial repolarization and tachyarrhythmia (ATA) in mice. Methods and Results In present study, the incidence of ATA were increased in Rgs5−/− Langendorff-perfused mouse hearts during program electrical stimulation (PES) (46.7%, 7 of 15) and burst pacing (26.7%, 4 of 15) compared with wild-type (WT) mice (PES: 7.1%,1 of 14; burst:7.1%,1 of 14) (P<0.05). And the duration of ATA also shown longer in Rgs5−/− heart than that in WT, 2 out of 15 hearts exhibited sustained ATA (>30 s) but none of them observed in WT mice. Atrial prolonged repolarization was observed in Rgs5−/− hearts including widened P wave in surface ECG recording, increased action potential duration (APD) and atrial effective refractory periods (AERP), all of them showed significant difference with WT mice (P<0.05). At the cellular level, whole-cell patch clamp recorded markedly decreased densities of repolarizing K+ currents including IKur (at +60 mV: 14.0±2.2 pF/pA) and Ito (at +60 mV: 16.7±1.3 pA/pF) in Rgs5−/− atrial cardiomyocytes, compared to those of WT mice (at +60 mV Ito: 20.4±2.0 pA/pF; Ikur: 17.9±2.0 pF/pA) (P<0.05). Conclusion These results suggest that Rgs5 is an important regulator of arrhythmogenesis in the mouse atrium and that the enhanced susceptibility to atrial tachyarrhythmias in Rgs5−/− mice may contribute to abnormalities of atrial repolarization.
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影响因子:
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作者:
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通讯作者:
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影响因子:
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作者:
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通讯作者:
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影响因子:
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作者:
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通讯作者:
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影响因子:
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作者:
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通讯作者:
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DOI:
10.1152/ajpheart.01400.2006
发表时间:
2007-08-01
影响因子:
4.8
作者:
Fischer, Robert;Dechend, Ralf;Schirdewan, Alexander
通讯作者:
Schirdewan, Alexander