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. 2021 Feb 10;8:607998. doi: 10.3389/fcvm.2021.607998

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Copyright © 2021 Simko and Baka.

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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Ivabradine's pleiotropic actions, along with heart rate (HR) reduction via I_f current inhibition, might mitigate neurohumoral activation, inflammation, oxidative stress, and atherosclerosis development, thus improving endothelial function and attenuating vascular remodeling and stiffness. These effects may contribute to endothelium-dependent and endothelium-independent vasodilation, potentially resulting in blood pressure (BP) reduction. Ald, aldosterone; Ang II, angiotensin II; AS, atherosclerotic; AT1, angiotensin II type 1 receptor; eNOS, endothelial nitric oxide synthase; HRV, heart rate variability; NA, noradrenaline; RAAS, renin–angiotensin–aldosterone system; SNS, sympathetic nervous system.