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. 2019 Dec 12;10:1493. doi: 10.3389/fphar.2019.01493

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Copyright © 2019 Ramalingam, Budin, Mohd. Fauzi, Ritchie and Zainalabidin

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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AT1 receptor antagonism attenuates nicotine-induced cardiomyocyte hypertrophy and fibrosis. Quantification of (A) cardiomyocyte cross-sectional area, cross-sectional area, and (B) collagen density in the left ventricular (LV) tissues with representative images of LV tissues stained with H&E or picrosirius red staining shown in (C). Relative gene expression of (D) atrial natriuretic peptide, (E) brain natriuretic peptide, (F) transforming growth factor β1, and (G) FN1 in LV tissues, normalized to 18S housekeeping gene after 4 weeks of nicotine administration. All values are given as mean ± SEM for n = 6 –7/group; *P < 0.05 vs. vehicle and ^# P < 0.05 vs. nicotine group using one-way ANOVA with Tukey post-hoc test.