Skip to main content
. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: J Mol Cell Cardiol. 2017 May 2;108:8–16. doi: 10.1016/j.yjmcc.2017.04.005

Figure 1. Proposed pathway for β-AR-induced increase of diastolic SR Ca2+ leak.

Figure 1

β-AR activation stimulates G-protein (Gs) dependent activation of adenylyl cyclase causing cAMP production that activates both Epac and PKA. The PKA branch enhances Ca2+ current (ICa) and phospholamban (PLB) sensitive SR Ca2+-ATPase (ATP). The Epac branch activates a cascade leading to NOS- and CaMKII-dependent RyR2 phosphorylation that promotes SR Ca2+ leak. Broken lines indicate a previously held idea that two parallel pathways might mediate Epac and NOS effects on RyR2.