U50,488H对正常及缺氧心肌细胞L型钙电流的作用

Effects of U50,488H on L-type calcium current in the normal and hypoxic rat ventricular myocytes

目的 探讨心脏阿片受体和β 受体相互作用的机制。方法 采用全细胞膜片钳技术 ,观察U5 0 ,4 88H(β 阿片受体选择性激动剂 )对正常和缺氧心肌细胞L型钙电流的作用。结果 U5 0 ,4 88H剂量依赖性(0 1～10 0 μmol/L)地抑制正常心肌细胞的L型钙电流及异丙肾上腺素(0 1μmol/L)激动的钙电流 ,而细胞缺氧后 ,这一抑制作用减弱 ;U5 0 ,4 88H对Forskolin(10 μmol/L)激动的L型钙电流无明显影响。结论 β 阿片受体对β 受体信号的负性调节作用在细胞缺氧后减弱 ,其作用位点可能发生于β 受体与腺苷酸环化酶环节之间。

Objective To explore the nechanism of the interaction between K-opioid receptor and β adrenal receptor. Method The effects of u50 488H on L-type calcium currents in the normal and hypoxic rat ventricular myocytes were studied by using whole-cell patch clamp technique. Results The basal as well as Isoproterenol-stimulated I_ Ca,L were inhibited by U50,488H in a dose-dependent manner in normal rat ventricular myocytes. In the hypoxic rat ventricular myocytes,the inhibitory effect of U50,488H was decreased. U50,488H had no significant effect on Forkolin-stimulated I_ Ca,L . Conclusion The results indicated that the negative modulation of β-opioid receptor on β-adrenoceptor was attenuated in the hypoxic ventricular myocytes,and the target of U50,488H on β-adrenergic system might be situated between β-adrenoceptor and adenylate cyclase.