Bisphenol A (BPA), an endocrine disrupting compound, has received much attention for its other probable health effects. It is a monomer of polycarbonate plastics, epoxy and polystyrene resins that are extensively used in the interior coating of cans in the food packaging industry and in dentistry. Human exposure to BPA occurs mainly through the ingestion of food and water from such containers and dental materials that leach BPA. Even though BPA is reported to produce reproductive and behavioural toxicity in experimental animals in various doses, the effect of BPA on the intestinal motility is not known till to date. The present study was designed to examine the effect of BPA on the movement of duodenum in vitro of rat. In this study, the movement of isolated duodenum of adult Sprague-Dawley rats (120-150gm, n=7) were recorded by isotonic transducer coupled to a RMS Polyrite-D machine (RMS Pvt. Ltd., India). The concentration-response of BPA on duodenal contraction was obtained in absence and presence of agonists and antagonists. Values are means±S.E.M. compared by Student’s t-test, p<0.05 vs. control and the treated preparations were expressed as percent change of the basal (or control) values. It was observed that BPA (10, 20, 40, 80, 160, 320µM) decreases the frequency (90.80±9.2, 84.80±4.9, 76.80±3.3, 55.20±2.2, 20.80±1, 2.4±0.4) and amplitude (66.66±3.2, 41.05±1.5, 39.3± 2.3, 35.84±2.2, 20.12±1.2, 9.3±1.3) of duodenal contraction in a dose-dependent manner. At last two doses (160µM and 320µM) the movement of duodenum were fully inhibited. Besides, BPA induced changes in duodenal movement was not blocked by atropine, the muscarinic receptor blocker. Further, BPA potentiated the inhibitory effect of the duodenal movement pre-treated with sodium nitroprusside (SNP, nitric oxide donor, 3.3 µM and 6.6µM). But the BPA induced inhibition of duodenal movement was blocked when the segment was pre-treated with L-NAME (nitric oxide synthase inhibitor, 90µM and 180µM) or methylene blue (MB, guanylyl cyclase inhibitor, 100 µM and 200 µM) (figure 1), and the blocking action of BPA was found to be fully reversed after 25,20,20 and 15 minutes respectively. It was also observed that phentolamine (3µM and 6µM), an α-adrenergic blocker, blocks the action of BPA upto the dose of 80µM (figure 2). But the BPA induced changes in the movement was not reversed by the propranolol, a β-adrenergic blocker. In other sets of experiments, equivalent doses of DMSO (solvent used for BPA) did not produce any change in the movement of isolated duodenum. From the results, it may be concluded that BPA inhibits the duodenal movement presumably by inducing nitric oxide mediated guanylyl cyclase and α-adrenergic signal pathways in duodenal smooth muscle cells.