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Changes in ion channel gene expression underlying heart failure-induced sinoatrial node dysfunction
Yanni J, Tellez JO, Maczewski M, Mackiewicz U, Beresewicz A, Billeter R, Dobrzynski H, Boyett MR
Circulation: Heart failure. 2011;4(4):496.
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Abstract
BACKGROUND: -Heart failure (HF) causes a decline in the function of the pacemaker of the heart, the sinoatrial node (SAN). The aim of the study was to investigate HF-induced changes in the expression of the ion channels and related proteins underlying the pacemaker activity of the SAN.METHODS AND RESULTS: -HF was induced in rats by the ligation of the proximal left coronary artery. HF animals showed an increase in the left ventricular diastolic pressure (317%) and a decrease in the left ventricular systolic pressure (19%) in comparison to sham-operated animals. They also showed SAN dysfunction: the intrinsic heart rate was reduced (16%) and the corrected SAN recovery time was increased (56%). qPCR was used to measure gene expression. During HF, of the 91 genes studied, 58% changed in the SAN, although only 1% changed in the atrial muscle. For example, there was an increase in the expression of ERG, K(v)LQT1, K(ir)2.4, TASK1, TWIK1/2, calsequestrin 2 and the A1 adenosine receptor in the SAN and this could explain the slowing of the intrinsic heart rate. In addition, there was an increase in NHE1 and this could be the stimulus for the remodelling of the SAN.CONCLUSIONS: -SAN dysfunction is associated with HF and is the result of an extensive remodelling of ion channels, gap junction channels, Ca(2+)-, Na(+)- and H(+)-handling proteins, and receptors in the SAN.PMID: 21565973 [PubMed - as supplied by publisher]