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Endogenous opioids have nitric oxide (NO)‐dependent cardiovascular actions. In the light of biological evidence of accumulation of endogenous opioids in cholestasis and also existence of NO‐dependent bradycardia in cholestatic subjects, this study was carried out to evaluate the role of endogenous opioids in the generation of bradycardia in a rat model of cholstasis. Male Sprague‐Dawley rats were used to induce cholestasis by surgical ligation of the bile duct, with sham‐operated animals serving as a control. The animals were divided into six groups which received naltrexone [20 mg/kg/day, subcutaneously (s.c.)], N^G‐l‐nitro‐arginine methyl ester (L‐NAME, 3 mg/kg/day, s.c.), aminoguanidine (200 mg/kg/day, s.c.), l‐arginine (200 mg/kg/day, s.c.), naltrexone + L‐NAME (20 and 3 mg/kg/day, s.c) or saline. One week after the operation, a lead II electrocardiogram (ECG) was recorded and the …