The vascular effects of aldosterone

Abstract

Aldosterone in addition to its synthesis in the zona glomerulosa of the adrenal gland is produced at the vascular level in both endothelial and smooth muscle cells1,2. This mineralocorticoid exerts actions in the vascular wall through genomic and non-genomic effects. Genomic actions imply the binding of aldosterone to cytoplasmatic mineralocorticoid receptors, which have been found in both endothelial and smooth muscle cells3-5 and involve transcription and protein synthesis3. The non-genomic effects of aldosterone are observed in a few minutes and are insensitive to transcription inhibitors, they seem to involve both mineralocorticoid and an unidentified membrane receptor2 and the activation of different signaling pathways. Numerous studies at both clinical and experimental levels have shown that this mineralocorticoid acting on endothelial cells or smooth muscle cells induces vascular alterations through endocrine and/or paracrine mechanisms which can affect vascular wall. The interaction of aldosterone to its receptors in endothelial cells produces swelling and stiffness. This increase in cell volume is associated with cell rigidity and produced numerous gaps between cell-to cell contacts6,7 which alters blood flow as well as vascular permeability and, consequently, can have an impact on vascular function and structure and can induce an inflammatory process.