Does aldosterone play a significant role for regulation of vascular tone? Aldosterone and vascular function

Kristina Sanne Lyngsø, Kasper Bostlund Assersen, Emil Geertsen Dalgaard, Ole Skøtt, Boye L. Jensen, Pernille B. Lærkegaard Hansen

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Besides the well-known renal effects of aldosterone, the hormone is now known to have direct vascular effects. Clinical observations underline substantial adverse effects of aldosterone on cardiovascular function. The source of systemic circulating aldosterone is the adrenal gland zona glomerulosa cells through stimulus-secretion coupling involving depolarization, opening of L- and T-type calcium channels and aldosterone synthase activation. Local formation and release in peripheral tissues such as perivascular fat is recognized. Where does aldosterone affect the vasculature? Mineralocorticoid receptors (MRs) are present in endothelial and vascular smooth muscle cells, and MR-independent pathways are also involved. The vascular effects of aldosterone are complex, both concentration and temporal and spatial aspects are relevant. The acute response includes vasodilation through endothelial nitric oxide formation and vasoconstrictor effects through endothelial-contracting cyclooxygenase-derived factors and a changed calcium handling. The response to aldosterone can change within the same blood vessels depending on the exposure time and status of the endothelium. Chronic responses involve changed levels of reactive oxygen radicals, endothelial Na-influx and smooth muscle calcium channel expression. Furthermore, perivascular cells for example mast cells have also been suggested to participate in the chronic response. Moreover, the vascular effect of aldosterone depends on the status of the endothelium which is likely the cause of the very different responses to aldosterone and MR treatment observed in human studies going from increased to decreased flow depending on whether the patient had prior cardiovascular disease with endothelial dysfunction or not. A preponderance of constrictor versus dilator responses to aldosterone could therefore be involved in the detrimental vascular actions of the hormone in the setting of endothelial dysfunction and contribute to explain the beneficial action of MR blockers on blood pressure and target organ injury.

Original languageEnglish
JournalJournal of Cardiovascular Pharmacology
Volume68
Issue number1
Pages (from-to)1-10
ISSN0160-2446
DOIs
Publication statusPublished - Jul 2016

Keywords

  • Blood vessels
  • Endothelial dysfunction
  • Aldosterone
  • Mineralocorticoid receptor
  • aldosterone
  • blood vessels
  • mineralocorticoid receptor
  • endothelial dysfunction
  • Aldosterone/metabolism
  • Endothelium, Vascular/metabolism
  • Humans
  • Mice, Transgenic
  • Mineralocorticoid Receptor Antagonists/therapeutic use
  • Nitric Oxide/metabolism
  • Signal Transduction/drug effects
  • Receptors, Mineralocorticoid/genetics
  • Vasodilation/drug effects
  • Muscle, Smooth, Vascular/metabolism
  • Prostaglandin-Endoperoxide Synthases/metabolism
  • Animals
  • Cardiovascular Diseases/drug therapy
  • Time Factors
  • Vasoconstriction/drug effects
  • Calcium Signaling

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