ReviewBritish journal of pharmacology2013
Aldosterone affects blood flow and vascular tone regulated by endothelium-derived NO: therapeutic implications.
Review in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 68 citations in OpenAlex.
- Acute effect of mineralocorticoid receptor antagonism on vascular function in healthy older adults.Experimental gerontology · 2016Trial
- SGK1 inhibition exerts atheroprotective effects in vascular endothelial cells.Biochemistry and biophysics reports · 2026Article
- Preliminary Exploration on Melatonin-Mediated Protective Effects in Intracranial Aneurysms: Transcriptomic, Proteomic, and Metabolomic Profiling of Cerebral Vascular Tissues Combined with in vivo Animal Experiments.Drug design, development and therapy · 2026Article
- Class A scavenger receptor MARCO negatively regulates Ace expression and aldosterone production.eLife · 2025Article
- Aldosterone and Cardiovascular Risk Across the Lifespan.Metabolites · 2025Review
- The relationship between aldosterone-induced retinal ganglion cell loss, blood pressure, and intraocular pressure.Japanese journal of ophthalmology · 2025Article
- MicroRNA-34a Mediates the Aldosterone-Induced Acceleration of Endothelial Senescence.International journal of hypertension · 2025Article
- Association of plasma aldosterone concentration with peripheral artery disease in hypertensive patients: insights from a large cross-sectional analysis.Frontiers in cardiovascular medicine · 2025Article
- Review Article on Molecular Mechanism of Regulation of Hypertension by Macro-elements (Na, K, Ca and Mg), Micro-elements/Trace Metals (Zn and Cu) and Toxic Elements (Pb and As).Biological trace element research · 2024Review
- Effects of Beraprost with or without NOS Inhibition on Plasma Aldosterone and Hemodynamics in Healthy Cats.Veterinary sciences · 2024Article
- A Selective Mineralocorticoid Receptor Blocker, Esaxerenone, Attenuates Vascular Dysfunction in Diabetic C57BL/6 Mice.Journal of atherosclerosis and thrombosis · 2023Article
- Review
- Article
- The Retinal Renin-Angiotensin-Aldosterone System: Implications for Glaucoma.Antioxidants (Basel, Switzerland) · 2022Article
- Analysis of potential functional significance of microRNA‑3613‑3p in human umbilical vein endothelial cells affected by heat stress.Molecular medicine reports · 2019Article
- Article
- Mineralocorticoid receptor deficiency improves the therapeutic effects of mesenchymal stem cells for myocardial infarction via enhanced cell survival.Journal of cellular and molecular medicine · 2019Article
- Changing views on the common physiologic abnormality that mediates salt sensitivity and initiation of salt-induced hypertension: Japanese research underpinning the vasodysfunction theory of salt sensitivity.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Review
- Collagen-Based Tissue Engineering Strategies for Vascular Medicine.Frontiers in bioengineering and biotechnology · 2019Review
- An experimental model for hypertensive crises emergencies: Long-term high-fat diet followed by acute vasoconstriction stress on spontaneously hypertensive rats.Experimental biology and medicine (Maywood, N.J.) · 2018Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aldosterone, in doses inappropriate to the salt status, plays an important role in the development of cardiovascular injury, including endothelial dysfunction, independent of its hypertensive effects. Acute non-genomic effects of aldosterone acting on mineralocorticoid receptors are inconsistent in healthy humans: vasoconstriction or forearm blood flow decrease via endothelial dysfunction, vasodilatation mediated by increased NO actions, or no effects. However, in studies with experimental animals, aldosterone mostly enhances vasodilatation mediated by endothelium-derived NO. Chronic exposure to aldosterone, which induces genomic responses, results in impairments of endothelial function through decreased NO synthesis and action in healthy individuals, experimental animals and isolated endothelial cells. Chronic aldosterone reduces NO release from isolated human endothelial cells only when extracellular sodium is raised. Oxidative stress is involved in the impairment of endothelial function by promoting NO degradation. Aldosterone liberates endothelin-1 (ET-1) from endothelial cells, which elicits ET(A) receptor-mediated vasoconstriction by inhibiting endothelial NO synthesis and action and through its own direct vasoconstrictor action. Ca(2+) flux through T-type Ca(2+) channels activates aldosterone synthesis and thus enhances unwanted effects of aldosterone on the endothelium. Mineralocorticoid receptor inhibitors, ET(A) receptor antagonists and T-type Ca(2) + channel blockers appear to diminish the pathophysiological participation of aldosterone in cardiovascular disease and exert beneficial actions on bioavailability of endothelium-derived NO, particularly in resistant hypertension and aldosteronism.
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