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. Author manuscript; available in PMC: 2012 Sep 14.
Published in final edited form as: Sci Transl Med. 2011 Sep 14;3(100):100ra88. doi: 10.1126/scitranslmed.3001909

Fig. 2.

Fig. 2

Resynchronization enhances β-receptor density and shifts signaling away from Gαi coupling to generate a Gαs-biased response. (A) β-Receptor maximal affinity binding (Bmax) reflecting surface membrane receptor abundance for combined and individual β1-AR and β2-AR subtypes. n = 4 for each group. *P < 0.05 versus other HF groups and control (within respective receptor group); †P < 0.01 versus β2-AR response. (B) Sarcomere shortening (%SS) and whole-cell calcium transient in cells from different models when stimulated with isoproterenol without or with pretreatment by pertussis toxin (PTX). PTX treatment greatly enhanced both behaviors in HFdys and HFsyn, but had no impact in resynchronized models. (C) %SS and peak Ca2+ transient in cells exposed to β2-AR–selective agonist zinterol (ZIN), zinterol + PTX, or the Gs-biased β2 agonist fenoterol. n = 12 to 20 cells per heart, and 3 to 4 hearts per group. *P < 0.01 versus other groups; †P < 0.001 versus zinterol; ‡P < 0.001 versus fenoterol.