Effects of b-adrenoceptor stimulation on delayed
Effects of b-adrenoceptor stimulation on delayed
复制标题
DOI：
--
复制
发表时间：
2011
期刊：
影响因子：
--
通讯作者：
G. Harmati;T. Bányász;L. Bárándi;N. Szentandrássy;B. Horváth;G. Szabó;Gábor Szénási;J. Magyar;P. Nanasi
中科院分区：
文献类型：
--
作者：
G. Harmati;T. Bányász;L. Bárándi;N. Szentandrássy;B. Horváth;G. Szabó;Gábor Szénási;J. Magyar;P. Nanasi
关键结果灌流ISO、Forsklin或细胞内应用PKA激活剂cAMP类似物(cAMP、8-BR-cAMP、6-BNZ-cAMP)后，IKR显著增加(30-50%)。RP-8-BR-cAMP抑制PKA对基线IKR无影响。选择性b1受体拮抗剂(美托洛尔和CGP-20712A)、PKA抑制剂RP-8-BR-cAMP和PKA激活剂cAMP类似物可完全抑制ISO对IKR的兴奋作用，而EPAC激动剂8-PCPT-2‘-O-Me-cAMP则不能。相比之下，激活PKA(ISO或8-BR-cAMP)可使IKs增加三倍，而PKA抑制剂RP-8-BR-cAMP则显著降低IKs。RP-8-BR-cAMP可减弱ISO对IKs的增强作用，8-BR-cAMP可完全抑制ISO对IKs的增强作用。
KEY RESULTS IKr was significantly increased (by 30–50%) following superfusion with ISO, forskolin or intracellular application of PKA activator cAMP analogues (cAMP, 8-Br-cAMP, 6-Bnz-cAMP). Inhibition of PKA by Rp-8-Br-cAMP had no effect on baseline IKr. The stimulating effect of ISO on IKr was completely inhibited by selective b1-adrenoceptor antagonists (metoprolol and CGP-20712A), by the PKA inhibitor Rp-8-Br-cAMP and by the PKA activator cAMP analogues, but not by the EPAC activator 8-pCPT-2’-O-Me-cAMP. In comparison, IKs was increased threefold by the activation of PKA (by ISO or 8-Br-cAMP), and strongly reduced by the PKA inhibitor Rp-8-Br-cAMP. The ISO-induced enhancement of IKs was decreased by Rp-8-Br-cAMP and completely inhibited by 8-Br-cAMP.