Introduction and Aims: The P1 and P2 receptors are expressed in cardiac tissue and activated by purines such as ATP, which are released by sympathetic neurons, endothelial cells and other tissues such as cardiomyocytes (Burnstock , G 2008). However, the role of these receptors in hypertension is still unclear. Therefore, this study proposed to investigate the role of the purinergic receptors and the signaling pathway on cardiac arrest induced by ATP in isolated right atria (RA) from normotensive (NWR) and spontaneously hypertensive rats (SHR). Materials and Methods: RA from NWR and SHR (4-6 months old) were isolated and mounted in isolated organ bath. The RA presented spontaneously beatings and the frequency between 220 and 520 bpm was considered as inclusion criterion. We study the effect of ATP (1 µM to 1 mM) on frequency of RA in the absence and presence of DPCPX (Dipropylcyclopentylxanthine) – a potent and selective antagonist for the adenosine A1 receptor (0.01 to 1 µM / pre-incubated for 20 min), 4-Aminopyridine – a potassium channel blocker (0.1 to 10 mM) and Bay k 8644 – which increases influx of calcium specifically at voltage-gated calcium channels (0.01 to 1µM). The results were analyzed by unpaired t test and one-way ANOVA. All experiments procedures were approved by the Ethics Committee of UNIFESP (n° 0778/11). Results: ATP (1 µM to 30 μM) produced an initial negative chronotropic effect (NCE) which lasted 60-90 s, followed by a negative inotropic effect (NIE) (n = 8). After that, the chronotropism gradually increased, showing a positive chronotropic effect (PCE) lasted 400 s followed by a positive inotropic effect (PIE). ATP 100 μM exerted in 40% of the experiments a biphasic effect. ATP 100 μM and 300 μM induced only a NCE in 60% and 100 % of the experiments, respectively. ATP 1 mM abolished the atrial contraction in SHR and NWR. The DPCPX (1 µM) blocked the NCE produced by ATP (300 µM) in 71.0 ± 1.3% (NWR) and 62.0 ± 1.2% (SHR) of the basal chronotropic effects. The DPCPX (1 µM) blocked the cardiac arrest produced by ATP (1 mM) in SHR and NWR. The 4-amino-pyridine (10 mM) and Bay k 8644 (1µM) blocked the cardiac arrest induced by ATP (1 mM). Conclusion: The results suggest that the cardiac arrest induced by ATP was due to the activation of A1 receptors followed by stimulation of outward K+ currents and blockade of inward Ca2+ currents in RA of NWR and SHR.