Effects of two dopaminergic agonists bromocriptine (BRO) and SKF-38393 (SKF) on electrophysiology of the ischemia-simulated rat atrial fibers with superfusion of modified physiologic salt solution (MPSS) were examined. All the action potential parameters were decreased or shortened during MPSS superfusion. APD90 (time for 90% repolarization) and dV/dtmax (maximum velocity of phase 0 depolarization), especially, were decreased markedly, up to 50% of the control. SKF (10-4 M) depolarized MDP (maximum diastolic potential) at 10 min, and increased dV/dtmax at 30 min superfusion of MPSS. APD90 was decreased at 10 min, inversely, and increased at 30 min superfusion of MPSS, directly proportional to the doses of SKF and BRO administered respectively. The APD-shortening effects at 10 min superfusion of MPSS were significantly enhanced by BRO (10-4 M), and the APD-shortening effects at 30 min superfusion of MPSS were significantly decreased by SKF (10-4 M). Haloperidol (3x10-6 M), a nonspecific dopaminergic antagonist, did not influence the effects of dopaminergic agonists on the APD-shortening of MPSS. Phentolamine (10-5 M), an alpha-adrenegic antagonist, significantly attenuated the BRO effects at 10 min superfusion of MPSS, and the SKF effects at 30 min MPSS superfusion were attenuated by propranolol (10-7 M), a beta-adrenergic antagonist. From these results, it is inferred that the dopaminegic agonists enhance or attenuate the APD-shortening effects during the ischemia-simulation, and that a part of enhancing effect by BRO is elicited through alpha-adrenergic receptors, whereas the attenuating effect by SKF is mediated partly by beta-adrenegic receptors.