The sinoatrial (SA) node is the primary pacemaker of the heart. It is known that SA node dysfunction is associated with increasing age (Di Gennaro et al. 1987). In addition, a reduction in intrinsic sinus rate is associated with heart failure (Janse et al. 2004). Ion channels and their associated subunits are key to the pacemaker function of the SA node. We used quantitative PCR to investigate if there is an age-dependent change in ion channel gene expression in the SA node. We separately investigated if heart failure causes a change in ion change gene expression in the SA node. For the study of ageing, 3 month (n=8) and 25 month (n=8) Wistar-Hanover rats were used. Heart failure was induced by generating an extensive myocardial infarction (caused by the ligation of the proximal left coronary artery performed under ketamine HCl and xylazine anaesthesia (100 mg/5 mg/kg body weight) injected intraperitoneally). Heart failure (n=8) and sham-operated (n=8) rats were used. In both studies, tissue was sampled from the right atrium and SA node (3 months post-operatively in the heart failure study). Ion channel gene expression was detected using quantitative PCR with an ABI 7900HT instrument with ABI Taqman probe assays. The study was conducted in accordance with Guide for the Care and Use of Laboratory Animals (US National Institutes of Health Publication No. 85-23, revised 1985). 82 gene transcripts were measured in the ageing study. Of these transcripts, with age 28% changed significantly in the atrial muscle and 23% changed in the SA node. In the SA node, these changes included significant increases in expression of transcripts responsible for Na_v1.5 (+33%) and Ca_v1.2 (+9%), which are responsible for the important inward currents, I_Na and I_Ca,L. With age, K_v1.2 (+61%) and K_v4.2 (+198%) transcript expression also increased in the SA node, whereas K_v1.5 (-40%) transcript expression decreased; these transcripts are responsible for important outward currents. 88 gene transcripts were measured in the heart failure study. Of these transcripts, with heart failure 7% changed significantly in the atrial muscle and 40% changed in the SA node. In the SA node, this included significant increases in expression of HCN4 (+63%), Ca_v1.2 (+55%) and Ca_v3.1 (+73%) transcripts, which are responsible for the important inward currents I_f, I_Ca,L and I_Ca,T. In addition, the expression of K_v1.2 (+72%) and K_v1.5 (+85%) transcripts, which are responsible for important outward currents, increased in the SA node in response to heart failure. These results show the dynamic nature of ion channel expression in the SA node. These results show that the expression of ion channels and their accessory subunits change in the SA node with age and during heart failure. These changes must contribute to the SA node dysfunction in the elderly and in heart failure.