【摘 要】
：
β-Adrenergic receptor (βAR) carries out the positive inotropic effect of the heart by enhancing L-type Ca2+ channel (LCC) Ca2+ influx and elevating sarcoplasmic reticulum (SR) Ca2+ release flux via ry
【机 构】
：
State Key Laboratory of Biomembrane and Membrane Biotechnology,Peking University,Beijing,China
【出 处】
：
International Conference for Physiological Sciences 2012(201
论文部分内容阅读
β-Adrenergic receptor (βAR) carries out the positive inotropic effect of the heart by enhancing L-type Ca2+ channel (LCC) Ca2+ influx and elevating sarcoplasmic reticulum (SR) Ca2+ release flux via ryanodine receptors (RyRs) through cAMP-PKA signaling pathway, but the exact contributions of β1-and β2-AR on the enhancement of LCC-RyR coupling have not been determined.By using the loose patch technique, we measured the response of a single RyR Ca2+ release unit, in form of a Ca2+ spark, to a Ca2+ sparklet from a single LCC.Selective β1AR stimulation increased Ca2+ spark amplitude, accelerated LCC-RyR response and increased the coupling fidelity.Oppositely, the β2AR agonist salbutamol can not alter spark amplitude or LCC-RyR coupling kinetics.However,β2AR stimulation still increased LCC current density in a cAMP-dependent manner, indicating a sufficient activation of β2AR-PKA pathway.At the intermolecular level, β2AR stimulation led to earlier start of Ca2+ sparks,which was attributed to enhanced LCC activity because of unaltered RyR gating kinetics.Between coupled LCCs and RyRs, only LCCs were modified under β2AR stimulation, exihibiting a nano-scale compartment of β2AR signaling.
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