Bisphenol A (BPA), an endocrine disruptor, is used in the manufacturing of plastics. BPA is reported to produce a number of reproductive defects and is even associated with behavioural abnormality, diabetes and deranged liver enzymes. However, the knowledge on toxic effects of BPA on cardiovascular system is limited. Therefore the present study was performed to examine the effects of BPA on spontaneously beating rat right atrial preparation in vitro as well as to see the changes after chronic exposure to BPA in in vivo conditions. The experiments were performed using adult female rats of Charles Foster strain weighing 150-200 grams after obtaining clearance from the ethical clearance committee of the institute. The study was divided in two groups. In group 1, in vitro isometric contractions of rat right atria were recorded. Effect of cumulative concentration of BPA on atrial contractions was obtained in the absence or presence of antagonists. BPA (0.1-100 μM) decreased the rate and the force of atrial contractions in a concentration dependent manner. The BPA-induced changes were blocked after pretreatment with N- ω- nitro-L- arginine methyl ester (L- NAME, a nitric oxide synthase inhibitor) or methylene blue (a guanylyl cyclase inhibitor) whereas atropine (muscarinic receptor blocker) did not block the BPA-induced changes in atria. In group 2, to study the effect of chronic exposure of BPA, the animals were ingested pellets with BPA (2 µg/kg body weight/day) or without BPA (time-matched control) for 30 days. Further, the animals were anaesthetized with urethane (1.5 gm/kg bw; i.p.) and prepared for recording blood pressure, ECG and respiratory excursions. Phenylbiguanide (PBG) 10 µg/kg body weight was injected through jugular vein to evoke cardio-pulmonary reflexes in these animals. Thereafter, the rats were killed using excess dose of urethane and the lungs and heart were excised and processed for histopathological examination. In time-matched control rats, PBG produced bradycardia, hypotension and tachypnoea over a period of time. In BPA treated group, the PBG-induced heart rate and respiratory frequency changes were attenuated significantly. The histological findings of the lungs revealed emphysematous and consolidative changes in BPA treated group whereas in case of heart, there was rupture of myofibrils with edematous changes. The present results indicate that BPA produces cardiac toxicity by producing acute and chronic changes. Acute changes were seen as decreased atrial contractility in vitro involving NO-dependent G-cyclase signaling mechanisms. The chronic changes manifested as lowered blood pressure and heart rate along with attenuation of cardio-respiraory reflexes. In addition there were degenerative changes in lungs and heart to produce the effects of chronic exposure.