文摘
In the cardio-vascular system extracellular UTP can induce receptor-mediated vasoconstriction via smooth muscle cells and vasodilatation via endothelial cells. We evaluated inotropic effects of UTP in preparations from human heart. Contractile effects were studied in atrial preparations from patients undergoing cardiac bypass surgery. For comparison, contractility in isolated spontaneously beating right atrial and paced left atrial preparations from mice was investigated. UTP and UTP纬S concentration-dependently exerted a positive inotropic effect with a maximum at 100 碌M UTP that amounted to 156% of pre-drug value (n=13) without changing time parameters of contraction. UTP was able to partially attenuate the positive inotropic effect of 尾-adrenoceptor stimulation. UTP did not change the beating rate in right atrial mouse preparations. The positive inotropic effect of UTP could not be blocked by the P2 purinoceptor antagonists suramin (100 碌M and 500 碌M), PPADS (50 碌M) and reactive blue (100 碌M). Likewise inhibitors of PLC activity (U73122) and of adenylyl cyclase activity (SQ22563; 10 碌M each) failed to affect the effects of UTP. In summary, we describe a novel positive inotropic effect of UTP on force contraction in the isolated human atrium. We tentatively suggest that UTP might act via P2Y2- or P2Y4-like receptors.