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. Author manuscript; available in PMC: 2011 Jun 11.
Published in final edited form as: Biochem Biophys Res Commun. 2010 May 10;396(4):921–926. doi: 10.1016/j.bbrc.2010.05.023

Figure 4. The PPARγ agonist troglitazone induces AT1AR-β-arrestin-dependent cardiomyocyte contractility.

Figure 4

(A) Isolated wild-type or βarr2-KO cardiomyocytes were field-stimulated at 0.5 Hz basally or following treatment with Ang II (10μM), Trog (50 or 100μM), Val (10μM) or ISO (1μM). Histograms summarize % (upper) and rate (lower) of cardiomyocyte shortening. †P<0.001 versus cells with no pharmacological treatment, n ≥ 3 individual hearts. (B) Comparison of the % change in contractility, relative to cells with no pharmacological treatment, in response to Ang II (10μM) or Trog (50 or 100μM) in wild-type versus βarr2-KO cardiomyocytes. *P<0.05 versus wild-type within corresponding treatment group.