Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (675 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A hormone secreted by the adrenal cortex that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Aldosterone, (+-)-Isomer; Aldosterone, (11 beta,17 alpha)-Isomer.
Where it fits in the MeSH classification
- Broader topics
- Pregnenediones; 11-Hydroxycorticosteroids
- See also
- Hyperaldosteronism; Hypoaldosteronism; Pseudohypoaldosteronism; Renin-Angiotensin System; Receptors, Mineralocorticoid
Related concepts
Research landscape
PubMed indexes 26,416 records tagged with the MeSH heading “Aldosterone” (counts retrieved 2026-10-31). 2,301 of them (8.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 17,032 records.
Reviews account for 2,872 records (10.9%) and meta-analyses for 69. Randomized controlled trials number 882 (3.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 17,032 |
| 2000-2009 | 3,602 |
| 2010-2019 | 3,481 |
| 2020 onward | 2,301 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,872 | 10.9% |
| Meta-analyses | 69 | 0.3% |
| Randomized controlled trials | 882 | 3.3% |
Method: PubMed query "Aldosterone"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Results from a phase 1, randomized, double-blind, multiple ascending dose study characterizing the pharmacokinetics and demonstrating the safety and selectivity of the aldosterone synthase inhibitor baxdrostat in healthy volunteers [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Baxdrostat is a selective inhibitor of aldosterone synthase designed for the treatment of disorders associated with elevated aldosterone.
- Closing excerpt
- The dose-dependent reduction in plasma aldosterone and lack of effect on cortisol demonstrate the selective blockade of aldosterone synthase.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (246 words)
Baxdrostat is a selective inhibitor of aldosterone synthase designed for the treatment of disorders associated with elevated aldosterone. This study evaluated the safety, pharmacokinetics, and pharmacodynamics of multiple ascending doses of baxdrostat in healthy volunteers. Subjects were randomized to receive oral baxdrostat (0.5, 1.5, 2.5, or 5.0 mg) or placebo once daily for 10 days and were placed on either a low-salt or normal-salt diet for the duration of the study. Blood samples were collected before and after dosing on days 1 and 10 to characterize pharmacokinetics and pharmacodynamics. Safety was assessed by adverse events, physical examinations, electrocardiograms, orthostatic vital signs, and clinical laboratory evaluations. Fifty-four subjects completed the study. There were no deaths or serious adverse events, and all treatment-emergent adverse events in subjects receiving baxdrostat were mild in severity. Plasma levels of baxdrostat increased proportionally with ascending doses, with peak concentrations observed within 4 h after dosing and a mean half-life of 26 to 31 h. A dose-dependent reduction of plasma aldosterone occurred with baxdrostat doses ≥1.5 mg, regardless of diet. Decreases in plasma aldosterone were sustained, with levels reduced by approximately 51 to 73% on day 10. Baxdrostat had no meaningful impact on plasma cortisol levels and resulted in mild dose-dependent decreases in plasma sodium levels and increases in potassium levels. Baxdrostat was safe and well tolerated with a half-life that supports once-daily dosing. The dose-dependent reduction in plasma aldosterone and lack of effect on cortisol demonstrate the selective blockade of aldosterone synthase.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36266539 · DOI · PMC9747611
Elevated aldosterone and blood pressure in a mouse model of familial hyperaldosteronism with ClC-2 mutation [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Gain-of-function mutations in the chloride channel ClC-2 were recently described as a cause of familial hyperaldosteronism type II (FH-II).
- Closing excerpt
- We demonstrate a role of ClC-2 in normal aldosterone production beyond the observed pathophysiology.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (134 words)
Gain-of-function mutations in the chloride channel ClC-2 were recently described as a cause of familial hyperaldosteronism type II (FH-II). Here, we report the generation of a mouse model carrying a missense mutation homologous to the most common FH-II-associated CLCN2 mutation. In these Clcn2R180Q/+ mice, adrenal morphology is normal, but Cyp11b2 expression and plasma aldosterone levels are elevated. Male Clcn2R180Q/+ mice have increased aldosterone:renin ratios as well as elevated blood pressure levels. The counterpart knockout model (Clcn2-/-), in contrast, requires elevated renin levels to maintain normal aldosterone levels. Adrenal slices of Clcn2R180Q/+ mice show increased calcium oscillatory activity. Together, our work provides a knockin mouse model with a mild form of primary aldosteronism, likely due to increased chloride efflux and depolarization. We demonstrate a role of ClC-2 in normal aldosterone production beyond the observed pathophysiology.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31727896 · DOI · PMC6856192
The Role of Aldosterone in OSA and OSA-Related Hypertension [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Obstructive sleep apnea (OSA) is regarded as an independent risk factor for hypertension.
- Closing excerpt
- Thus, a bidirectional influence between OSA and aldosterone exists and contributes to hypertension in OSA patients, especially resistant hypertension.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (108 words)
Obstructive sleep apnea (OSA) is regarded as an independent risk factor for hypertension. The possible mechanism includes oxidative stress, endothelial injury, sympathetic excitement, renin-angiotensin-aldosterone system activation, etc. Clinical studies have found that there is a high coexistence of OSA and primary aldosteronism in patients with hypertension and that elevated aldosterone levels are independently associated with OSA severity in resistant hypertension. The underlying mechanism is that aldosterone excess can exacerbate OSA through increasing overnight fluid shift and affecting the mass and function of upper airway muscles during the sleep period. Thus, a bidirectional influence between OSA and aldosterone exists and contributes to hypertension in OSA patients, especially resistant hypertension.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35095768 · DOI · PMC8791261
Integrated Transcriptomics Reveals Evolutionary Trajectories and Cell Density-Dependent Mechanisms in Aldosterone-Producing Adenomas [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Aldosterone-producing adenomas (APAs) and micronodules (APMs) are histopathological lesions that can cause a prevalent form of secondary hypertension called primary aldosteronism.
- Closing excerpt
- The findings enhance understanding of the transcriptional diversity in APMs and APAs and elucidate complex molecular alterations underlying APA pathogenesis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (187 words)
Aldosterone-producing adenomas (APAs) and micronodules (APMs) are histopathological lesions that can cause a prevalent form of secondary hypertension called primary aldosteronism. Using integrated single-cell/nucleus and spatial transcriptomics, it demonstrates substantial heterogeneity between APMs and APAs, alongside an immunosuppressive tumor microenvironment in APAs. Pseudotime analyses reveal two distinct evolutionary trajectories in APAs: a direct progression from zona glomerulosa cells to APAs, observed specifically in KCNJ5-mutated tumors, and a stepwise path from zona glomerulosa cells to APMs and then to APAs, present in both KCNJ5-mutated APAs and APAs without KCNJ5 mutations. Within KCNJ5-mutated APAs, we identified two distinct cellular states with different differentiation potentials: a progenitor-like state (high differentiation potential) and a mature state (low differentiation potential). This uncovered a spectrum of molecular and functional shifts during APA progression involving pathways of oxidative stress (including mechanisms leading to cell death by ferroptosis) and focal adhesion (influenced by cell density). In vitro studies in human adrenal cells demonstrate that TAZ activation regulates ferroptosis sensitivity in response to cell density changes. The findings enhance understanding of the transcriptional diversity in APMs and APAs and elucidate complex molecular alterations underlying APA pathogenesis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41562146 · DOI · PMC13252614
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Hypertension: renin-angiotensin-aldosterone system alterations [5]
- Research article Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: A novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis [6]
- Research article Aldosterone, Inflammation, Immune System, and Hypertension [7]
- Research article Aldosterone and end-organ damage [8]
- Research article Role of Renin-Angiotensin-Aldosterone System Activation in Promoting Cardiovascular Fibrosis and Stiffness [9]
- Research article Primary Aldosteronism: JACC State-of-the-Art Review [10]
References
- Freeman MW, Bond M, Murphy B, Hui J, Isaacsohn J. Results from a phase 1, randomized, double-blind, multiple ascending dose study characterizing the pharmacokinetics and demonstrating the safety and selectivity of the aldosterone synthase inhibitor baxdrostat in healthy volunteers. . 2023. PMID 36266539 · DOI · PMC9747611
- Schewe J, Seidel E, Forslund S, Marko L, Peters J, Muller DN, et al.. Elevated aldosterone and blood pressure in a mouse model of familial hyperaldosteronism with ClC-2 mutation. . 2019. PMID 31727896 · DOI · PMC6856192
- Wang Y, Li CX, Lin YN, Zhang LY, Li SQ, Zhang L, et al.. The Role of Aldosterone in OSA and OSA-Related Hypertension. . 2021. PMID 35095768 · DOI · PMC8791261
- Sun Z, Jing C, Tetti M, Gong S, Wei J, Pang Y, et al.. Integrated Transcriptomics Reveals Evolutionary Trajectories and Cell Density-Dependent Mechanisms in Aldosterone-Producing Adenomas. . 2026. PMID 41562146 · DOI · PMC13252614
- Te Riet L, van Esch JH, Roks AJ, van den Meiracker AH, Danser AH. Hypertension: renin-angiotensin-aldosterone system alterations. Circ Res. 2015. PMID 25767283 · DOI
- Henry BM, Vikse J, Benoit S, Favaloro EJ, Lippi G. Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: A novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis. Clin Chim Acta. 2020. PMID 32348783 · DOI · PMC7195008
- Ferreira NS, Tostes RC, Paradis P, Schiffrin EL. Aldosterone, Inflammation, Immune System, and Hypertension. Am J Hypertens. 2021. PMID 32820797 · DOI · PMC7891246
- Marney AM, Brown NJ. Aldosterone and end-organ damage. Clin Sci (Lond). 2007. PMID 17683282 · DOI
- Jia G, Aroor AR, Hill MA, Sowers JR. Role of Renin-Angiotensin-Aldosterone System Activation in Promoting Cardiovascular Fibrosis and Stiffness. Hypertension. 2018. PMID 29987104 · DOI · PMC6202147
- Rossi GP. Primary Aldosteronism: JACC State-of-the-Art Review. J Am Coll Cardiol. 2019. PMID 31779795 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.