ReviewCurrent hypertension reports2015
Activation of mineralocorticoid receptor in salt-sensitive hypertension.
Review in Current hypertension reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 24 citations in OpenAlex.
- Associations of Genetic Variations in the NR3C2 With Salt Sensitivity, Longitudinal Blood Pressure Changes, and Incidence of Hypertension in Chinese Adults.Journal of clinical hypertension (Greenwich, Conn.) · 2025Observational
- Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase.American journal of physiology. Renal physiology · 2024Article
- Characteristics and variation of fecal bacterial communities and functions in isolated systolic and diastolic hypertensive patients.BMC microbiology · 2021Article
- Aldosterone Regulates Pendrin and Epithelial Sodium Channel Activity through Intercalated Cell Mineralocorticoid Receptor-Dependent and -Independent Mechanisms over a Wide Range in Serum Potassium.Journal of the American Society of Nephrology : JASN · 2020Article
- Renal intercalated cells and blood pressure regulation.Kidney research and clinical practice · 2017Review
- Salt-dependent Blood Pressure in Human Aldosterone Synthase-Transgenic Mice.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The impaired capacity of the kidney to excrete sodium plays an essential role in the development of hypertension. Adrenal corticosteroids control renal handling of sodium by regulating tubular sodium reabsorption in the distal nephron where both mineralocorticoid receptors (MR) and glucocorticoid receptors are expressed. In addition, cell type- and segment-specific expression of 11β-HSD2 and sodium transporters such as Na-Cl cotransporter (NCC), epithelial sodium channel (ENaC), and pendrin/Na(+)-driven Cl(-)/HCO3 (-) exchanger (NDCBE) builds a distinctive model of sodium transport in the aldosterone-sensitive distal nephron. Aberrant MR activation in the distal nephron triggers salt-sensitive hypertension and hypokalemia through inappropriate sodium reabsorption and potassium secretion. However, MR activity is not necessarily modulated by the ligand alone. Recently, several lines of evidence revealed alternative mechanisms that regulate the activity of MR in a ligand-independent manner or through ligand binding modulation. This review summarizes the disorders related to MR activation in individual tubular cells and highlights the renal mechanism of salt-sensitive hypertension and new approaches for the prevention and treatment of this disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.