title: Atrial tachyarrhythmia in Rgs5-null mice.
abstract: OBJECTIVE
  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.
  
  
  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 I(Kur) (at +60 mV: 14.0±2.2 pF/pA) and I(to) (at +60 mV: 16.7±1.3 pA/pF) in Rgs5(-/-) atrial cardiomyocytes, compared to those of WT mice (at +60 mV I(to): 20.4±2.0 pA/pF; I(kur): 17.9±2.0 pF/pA) (P<0.05).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: Mu
authors.initials: M
authors.lastname: Qin
authors.forename: He
authors.initials: H
authors.lastname: Huang
authors.forename: Teng
authors.initials: T
authors.lastname: Wang
authors.forename: He
authors.initials: H
authors.lastname: Hu
authors.forename: Yu
authors.initials: Y
authors.lastname: Liu
authors.forename: Yongwei
authors.initials: Y
authors.lastname: Gu
authors.forename: Hong
authors.initials: H
authors.lastname: Cao
authors.forename: Hongliang
authors.initials: H
authors.lastname: Li
authors.forename: Congxin
authors.initials: C
authors.lastname: Huang
mesh_terms: D000200:Action Potentials; D000818:Animals; D002478:Cells, Cultured; D017353:Gene Deletion; D006321:Heart / Q000503:physiopathology*; D006325:Heart Atria / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D018408:Patch-Clamp Techniques; D020710:RGS Proteins / Q000235:genetics* / Q000378:metabolism; D013610:Tachycardia / Q000235:genetics* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
chemical_list: D020710:RGS Proteins; C105346:Rgs5 protein, mouse