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. 2011 Aug;25(8):2583–2591. doi: 10.1096/fj.11-184622

Figure 3.

Figure 3.

Blunted inotropic response to adrenergic stimulation in cardiomyocytes lacking ERO1α. A) Left panels: calcium transients in electrically paced (0.5 Hz) freshly isolated wild-type (WT) or Ero1α mutant (Ero1α mut) cardiomyocytes after exposure to the adrenergic agonist isoproterenol (30 nM). Right panel: superimposed tracings from WT (black) and Ero1α mut (red) adult cardiomyocytes, normalized to the same peak amplitude. B) Graphic presentation of the mean peak amplitude of the calcium transient (normalized to an average value of 1 for WT cardiomyocytes), τ, and sarcomere length in the 2 genotypes after adrenergic stimulation. C) Peak amplitude of the caffeine-induced calcium transient (normalized to an average value of 1 for WT cardiomyocytes) in the absence (−) and presence (+) of isoproterenol (ISO). D) Graphic presentation of the mean peak amplitude of the calcium transient, τ, and sarcomere length before (−) and after (+) adrenergic stimulation in cardiomyocytes from WT, Ero1α mutant (α mut), and compound Ero1α; Ero1β mutant mice (αβ mut). Data are presented as means ± se; number of cells studied is indicated. *P < 0.05, **P < 0.01.