|Title:||Endothelial dysfunction in primary aldosteronism||Authors:||ZHENG-WEI CHEN
TAIPAI Study Group
|Issue Date:||2019||Journal Volume:||20||Journal Issue:||20||Start page/Pages:||5214||Source:||International Journal of Molecular Sciences||Abstract:||
Primary aldosteronism (PA) is characterized by excess production of aldosterone from the adrenal glands and is the most common and treatable cause of secondary hypertension. Aldosterone is a mineralocorticoid hormone that participates in the regulation of electrolyte balance, blood pressure, and tissue remodeling. The excess of aldosterone caused by PA results in an increase in cardiovascular and cerebrovascular complications, including coronary artery disease, myocardial infarction, stroke, transient ischemic attack, and even arrhythmia and heart failure. Endothelial dysfunction is a well-established fundamental cause of cardiovascular diseases and also a predictor of worse clinical outcomes. Accumulating evidence indicates that aldosterone plays an important role in the initiation and progression of endothelial dysfunction. Several mechanisms have been shown to contribute to aldosterone-induced endothelial dysfunction, including aldosterone-mediated vascular tone dysfunction, aldosterone-and endothelium-mediated vascular inflammation, aldosterone-related atherosclerosis, and vascular remodeling. These mechanisms are activated by aldosterone through genomic and nongenomic pathways in mineralocorticoid receptor-dependent and independent manners. In addition, other cells have also been shown to participate in these mechanisms. The complex interactions among endothelium, inflammatory cells, vascular smooth muscle cells and fibroblasts are crucial for aldosterone-mediated endothelial dysregulation. In this review, we discuss the association between aldosterone and endothelial function and the complex mechanisms from a molecular aspect. Furthermore, we also review current clinical research of endothelial dysfunction in patients with PA. ? 2019 by the authors. Licensee MDPI, Basel, Switzerland.
|URI:||https://scholars.lib.ntu.edu.tw/handle/123456789/479398||ISSN:||1661-6596||DOI:||10.3390/ijms20205214||SDG/Keyword:||calcium activated potassium channel; epidermal growth factor receptor; epithelial sodium channel; eplerenone; G protein coupled receptor 30; glucose 6 phosphate dehydrogenase; nitric oxide; oxidoreductase; prostaglandin synthase; Rho kinase; vasoconstrictor agent; aldosterone; atherosclerosis; blood vessel tone; cardiovascular disease; cell interaction; disease exacerbation; endothelial dysfunction; endothelial progenitor cell; endothelium; exosome; fibroblast; gene mutation; human; hyperaldosteronism; hypertension; inflammation; inflammatory cell; nonhuman; protein phosphorylation; Review; vascular remodeling; vascular smooth muscle cell; vasculitis; vasoconstriction; vasodilatation; vasomotor reflex; cardiovascular disease; cerebrovascular disease; complication; hyperaldosteronism; metabolism; signal transduction; Aldosterone; Cardiovascular Diseases; Cerebrovascular Disorders; Disease Progression; Humans; Hyperaldosteronism; Signal Transduction
|Appears in Collections:||醫學院附設醫院 (臺大醫院)|
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