Skip to main content
. Author manuscript; available in PMC: 2022 Jan 22.
Published in final edited form as: Circ Res. 2020 Nov 13;128(2):246–261. doi: 10.1161/CIRCRESAHA.120.317452

Figure 7. Deletion of OCT3 reduces catecholamine uptake, cAMP signal and inotropic response in response to adrenergic stimulation of mouse hearts.

Figure 7.

(A) Heart weight/body weight ratio (HW/BW %) in WT and OCT3-KO mice. Data are shown as mean ± S.E.M. (N = 8). p values were obtained by student t-test. (B, C) Quantitative determination of endogenous NE in cardiac tissues and the plasma. Data are shown as mean ± S.E.M. (N = 8). p values were obtained by student t-test. (D) Quantitative determination of cAMP levels in cardiac tissues. Data are shown as mean ± S.E.M. (N = 4). p values were obtained by student t-test. (E) Representative echocardiographic images of WT (N = 7) and OCT3KO (N = 6) mice at baseline and after intraperitoneal injection of 10 μg/kg isoproterenol (ISO) or epinephrine (EPI). (F-I) Cardiac ejection fraction (EF) of individual mice before and after intraperitoneal injection of ISO or EPI in WT (N = 7) and OCT3KO (N = 6). Quantification of EF and heart rate (HR) in WT and OCT3KO mice before and after injection with ISO or EPI. Data are shown as mean ± S.E.M. p values were obtained by two-way ANOVA analysis with Tukey’s multiple comparison test.