Objective: In this study, the effect of agmatine was studied on sympathetic neurotransmission in the frog isolated ventricular strips. Methods: Ventricular strips were prepared from the heart of the pitched frog. Each strip was mounted vertically in an organ bath. Musc- le contractions were recorded isometrically by a force displacement transducer and displayed on a polygraph. Results: Concentration-response relationships to noradrenaline were obtained on contractility of frog ventricular strips evoked by elect- rical stimulation. The responses of noradrenaline were re-obtained in presence of agmatine (3X10-4 M). Agmatine was found to be inef- fective on contractile responses of noradrenaline in electrically driven ventricular strips of frog heart. Transient additional stimulations (TAS) induced contractions. The contractions induced by TAS were re-obtained in presence of agmatine, idazoxan + agmatine and yo- himbine + agmatine. Agmatine significantly increased the positive inotropic responses of TAS. The effect of agmatine on contractile res- ponses of TAS was not changed by idazoxan, indicating that imidazoline receptors have not functions in this response. The effect of ag- matine on the contractile responses to TAS was reversed by yohimbine, indicating involvement of α2 adrenoceptors in this response. Ag- matine did not change the contractile responses of ventricular strips to exogenous noradrenaline, indicating that agmatine does not af- fect postjunctional adrenoceptors. Conclusion: These results suggest that agmatine facilitates sympathetic neurotransmission in frog myocardium via an action on prejunc- tional α2 adrenergic receptors located on sympathetic nerve terminals.