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. 2010 May 21;299(2):H322–H331. doi: 10.1152/ajpheart.00392.2010

Fig. 6.

Fig. 6.

β1-AR antagonists abolished ISO-induced myocyte death, while β2-AR stimulation exerted significant protection against myocyte death in WT mice. A and B: for WT and TG myocyte viability, respectively, at 12 h, ISO + NIF treatment caused a greater myocyte viability compared with NIF alone, and the effect was inhibited by the β2-AR antagonist ICI 118551 (ICI; N = 4). C and D: WT and TG myocyte viability, respectively, at 12 h after treatment with β-AR subtype activators and inhibitors (N = 6). Values are means ± SE. ZIN, zinterol, a β2-AR selective agonist; CGP, CGP 20712A, a β1-AR antagonist; ICI is a β2-AR antagonist; DOB, dobutamine, a β1-AR selective agonist; NIF is an LTCC antagonist. *P < 0.05 vs. CON. #P < 0.05, Zin + CGP vs. CGP. &P < 0.05, ISO + ICI vs. ICI. ∧P < 0.05, DOB vs. DOB + CGP. $P < 0.05, ISO + CGP vs. ISO. @P < 0.05, ISO+NIF vs. NIF. %P < 0.05, ISO + NIF + ICI vs. ISO + NIF.