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. 2013 Jun 21;2(3):e000150. doi: 10.1161/JAHA.113.000150

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© 2013 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley-Blackwell.

This is an Open Access article under the terms of the Creative Commons Attribution Noncommercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 3. — Effects of ivabradine (iva) on the gene expression in dnNRSF‐Tg (Tg) mice. A through F, Relative levels of ANP (A), BNP (B), SERCA2 (C), HCN2 (D), HCN4 (E), and CACNA1H (F) mRNA in hearts from 20‐week‐old WT and Tg mice treated with or without iva. n=3 in each group. Mice treated without iva are indicated as cont. Kruskal–Wallis nonparametric ANOVA followed by the Bonferroni correction was used for analysis among the 4 groups. All data are shown as dot plots. NS indicates not significant; ANP, atrial natriuretic peptide; cont, control; WT, wild type; dnNRSF‐Tg, dominant‐negative form of neuron‐restrictive silencer factor in transgenic mice; BNP, brain natriuretic peptide; SERCA2, sarcoplasmic/endoplasmic reticulum calcium ATPase 2; HCN2, hyperpolarization‐activated cyclic nucleotide‐gated channel 2; CACNA1H, calcium channel, voltage‐dependent, T type, alpha 1H subunit; ANOVA, analysis of variance.