ISSN |
1949-8462 (online) |
Open Access |
This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ |
Copyright |
© The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved. |
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Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
Website |
http://www.wjgnet.com |
Category |
Cardiac & Cardiovascular Systems |
Manuscript Type |
Basic Study |
Article Title |
Nicotine-induced adrenal beta-arrestin1 upregulation mediates tobacco-related hyperaldosteronism leading to cardiac dysfunction
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Manuscript Source |
Invited Manuscript |
All Author List |
Natalie Cora, Jennifer Ghandour, Celina Marie Pollard, Victoria Lynn Desimine, Krysten Elaine Ferraino, Janelle Marie Pereyra, Rachel Valiente and Anastasios Lymperopoulos |
ORCID |
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Funding Agency and Grant Number |
Funding Agency |
Grant Number |
AFPE |
333325 |
Nova Southeastern University |
PFRDG 335467 |
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Corresponding Author |
Anastasios Lymperopoulos, BPharm, FAHA, MSc, PhD, Associate Professor, Director, Director, Laboratory for the Study of Neurohormonal Control of the Circulation, Department of Pharmaceutical Sciences (Pharmacology), College of Pharmacy, Nova Southeastern University, 3200 S. University Dr., HPD (Terry) Bldg/Room 1338, Fort Lauderdale, FL 33328-2018, United States. al806@nova.edu |
Key Words |
Adrenocortical zona glomerulosa cell; Aldosterone; Beta-arrestin; Nicotine; Signal transduction; Tobacco-related heart disease |
Core Tip |
Adrenal arrestin1 is a novel molecular target for mitigation of the aldosterone-dependent cardiotoxic effects of tobacco. Angiotensin II (AngII) induces aldosterone production in adrenocortical zona glomerulosa (AZG) cells by binding to its adrenal AngII type 1 receptor (AT1R), which then activates arrestin1. Nicotine and cotinine are known to activate the renin-angiotensin-aldosterone-system (RAAS), promoting hyperaldosteronism. We report herein that these main tobacco compounds chronically upregulate adrenal arrestin1, promoting excessive aldosterone synthesis and secretion from human AZG cells in vitro and from adrenal glands in vivo. Thus, adrenal arrestin1 critically mediates tobacco-induced RAAS activation, which contributes to heart disease development/progression. |
Publish Date |
2020-05-26 02:23 |
Citation |
Cora N, Ghandour J, Pollard CM, Desimine VL, Ferraino KE, Pereyra JM, Valiente R, Lymperopoulos A. Nicotine-induced adrenal beta-arrestin1 upregulation mediates tobacco-related hyperaldosteronism leading to cardiac dysfunction. World J Cardiol 2020; 12(5): 192-202 |
URL |
https://www.wjgnet.com/1949-8462/full/v12/i5/192.htm |
DOI |
https://dx.doi.org/10.4330/wjc.v12.i5.192 |