Synergistic action of neuropeptide Y and adrenaline in the eel atrium.

To investigate the influence of neuropeptide Y (NPY) on heart function in a relatively simple model system, the effects of eel NPY (eNPY) on the eel atrium were examined. Eel NPY enhanced the contractile force of the isolated atrium in a dose-dependent manner, without altering the rate of contraction. Although adrenaline also exerts a positive inotropic effect, the effect of eNPY was not blocked by the beta 1-adrenoceptor antagonist betaxolol, indicating that eNPY does not act via adrenaline release. When eNPY and adrenaline were applied simultaneously, their effects were additive at lower concentrations but not at higher concentrations. The plateau reached at high concentrations suggests that these two regulators act through a common signal transduction process. One candidate for this is an elevation of the concentration of intracellular free Ca2+ ([Ca2+]i), since treatment with eNPY or adrenaline enhanced [Ca2+]i, as assessed by fluorescence of Calcium Green-1. The increase in [Ca2+]i after eNPY and adrenaline treatment is presumably due to Ca2+ influx from the external medium, since the effect was greatly reduced in Ca(2+)-free Ringer's solution and after treatment with verapamil, a Ca2+ channel blocker. Although both eNPY and adrenaline enhanced the atrial contractile force, the time courses were different, with the effect of eNPY being gradual and long-lasting, and that of adrenaline being immediate and transient. It is plausible, therefore, that eNPY and catecholamine(s) act synergistically to cause a long-lasting enhancement of contraction force if the two regulators arrive at the atrium simultaneously. The present study also demonstrates that the eel heart contains eNPY.