Agmatine facilitates sympathetic neurotransmission in frog myocardium via an action on alfa 2-adrenergic receptors

Abstract

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. Muscle 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 electrical stimulation. The responses of noradrenaline were re-obtained in presence of agmatine (3×10-4 M). Agmatine was found to be ineffective 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 yohimbine + agmatine. Agmatine significantly increased the positive inotropic responses of TAS. The effect of agmatine on contractile responses of TAS was not changed by idazoxan, indicating that imidazoline receptors have not functions in this response. The effect of agmatine on the contractile responses to TAS was reversed by yohimbine, indicating involvement of ?2 adrenoceptors in this response. Agmatine did not change the contractile responses of ventricular strips to exogenous noradrenaline, indicating that agmatine does not affect postjunctional adrenoceptors. Conclusion: These results suggest that agmatine facilitates sympathetic neurotransmission in frog myocardium via an action on prejunctional ?2 adrenergic receptors located on sympathetic nerve terminals.