Component
Rat serum aldosterone concentration
The hormone readout in this model, recorded as a measurement rather than as the hormone itself.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Serum aldosterone was significantly lower in cyclosporine-treated rats, and the authors read the fall in the sodium-chloride cotransporter as following an inactivated renin-angiotensin-aldosterone system.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Rat model of cyclosporine nephrotoxicity
- exposure
- Cyclosporine, dose and duration not stated here
- limitations
- A hormone measurement in rats. The link from the lower aldosterone to the lower cotransporter is the authors' interpretation of two associated findings.
- organism
- Rat model of cyclosporine nephrotoxicity
- plain_language
- Serum aldosterone was significantly lower in cyclosporine-treated rats, and the authors read the fall in the sodium-chloride cotransporter as following an inactivated renin-angiotensin-aldosterone system.
- primary_references
- Expression of renal distal tubule transporters TRPM6 and NCC in a rat model of cyclosporine nephrotoxicity and effect of EGF treatment. (2011). https://pubmed.ncbi.nlm.nih.gov/21653632/ DOI: 10.1152/ajprenal.00116.2011
- route
- In vivo
- tissue
- Renin-angiotensin-aldosterone system
Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 322–322
Original AI-assisted curation of seven primary studies resolved by PubMed title search, with every abstract read and all DOIs cross-checked against live PubMed metadata on 2026-09-23. No reference carries a recorded retraction, erratum or expression of concern. Each of the seven is a separate laboratory and each carries its own lineage key, so none of them can be counted twice as independent support. Study-specific concentrations, kinetic constants and limitations retained. Not publisher full text. · supports · Rat model of cyclosporine nephrotoxicity · source_derived_draft · unverified_draft
Serum aldosterone was significantly lower in cyclosporine-treated rats, and the authors read the fall in the sodium-chloride cotransporter as following an inactivated renin-angiotensin-aldosterone system.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.