摘要
目的研究起搏离子流If的调控机制。方法运用穿孔膜片箝技术，在游离的兔心窦房结细胞上进行研究。结果1．蛋白激酶抑制剂H－7使If减小，而蛋白磷酸酶抑制剂有增强If作用，表明磷酸化过程参与If的调控。2．阻断PKA途径后，β受体激动时，仍有增加If的作用，证实了cAMP对If通道有直接作用。3．运用cAMP的同分异构体Rp－cAMP（Rp）和Sp-cAMP（Sp），其中Sp由于具有激活蛋白激酶的作用，其较Rp有更强的调控If的作用。结论β受体激动是通过cAMP对门控直接作用及PKA磷酸化间接作用二种途径来完成对起搏离子流If的调控。
ObjectiFe Study the regulatory mechanism of pacemaker current If. MethodsPerforated patch clamp techniques were employed on isolated rabbit SN cells. Results 1.The non - specific protein kinase inhibitor H - 7 reversibly reduced the magnitude of If, whilecalyculin A, a non- specific phosphatase inhibitor reversibly increased If in 5 SAN cells,which demonstrate that phosphorylation take part in the regulati0n of If. 2. When PKA wasinhibited by H - 8, isoproterenol still increased If, which suggest the direct gating of cAMP.3. Comparing the actions of the Rp and Sp isomers of cAMP rap does not activate the Akinase, while Sp does) indicates that Sp has larger effect, Conclusion The actions of betaagitation appear to be mediated by both phosph0rylation and direct cAMP gating.
出处
《上海第二医科大学学报》
CSCD
1999年第3期231-233,共3页
Acta Universitatis Medicinalis Secondae Shanghai
基金
国家自然科学基金!39870779
上海高校科技发展基金!98BJ02
