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.