Component
Rat collecting-duct aquaporin-2 / Aqp2
Rat collecting-duct aquaporin-2 / Aqp2. Species, exposure and limitations are retained in each linked claim.
2 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.
Where it participates (unsigned role)
Vasopressin increased apical AQP2 labeling and shifted AQP2 from intracellular vesicles toward the apical membrane.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/7532304.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4", "start_char": 0, "end_char": 1588, "text_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4"}
- experimental_model
- Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy
- exposure
- Vasopressin addition and withdrawal
- limitations
- Direct water-channel trafficking experiment; no claim that sodium dietary deficiency caused the response.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Rat
- plain_language
- The kidney can retain more water by moving water channels to the cell surface.
- primary_references
- [sodium-p7532304] Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. (1995). https://pubmed.ncbi.nlm.nih.gov/7532304/ DOI: 10.1073/pnas.92.4.1013
- tissue_or_cell_type
- Inner medullary collecting duct
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 421–432
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy · source_derived_draft · unverified_draft
### sodium-avp-aqp2 Vasopressin increased apical AQP2 labeling and shifted AQP2 from intracellular vesicles toward the apical membrane. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney can retain more water by moving water channels to the cell surface. organism: Rat tissue_or_cell_type: Inner medullary collecting duct experimental_model: Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy limitations: Direct water-channel trafficking experiment; no claim that sodium dietary deficiency caused the response. exposure: Vasopressin addition and withdrawal evidence_span: {"source_cache": "artifacts/sodium-research/7532304.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4", "start_char": 0, "end_char": 1588, "text_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4"} [sodium-p7532304] Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. (1995). https://pubmed.ncbi.nlm.nih.gov/7532304/ DOI: 10.1073/pnas.92.4.1013
Complete structured claim and evidenceWater permeability rose during vasopressin exposure and fell after withdrawal in parallel with AQP2 redistribution.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/7532304.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4", "start_char": 0, "end_char": 1588, "text_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4"}
- experimental_model
- Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy
- exposure
- Vasopressin addition and withdrawal
- limitations
- Direct water-channel trafficking experiment; no claim that sodium dietary deficiency caused the response.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Rat
- plain_language
- This is a water-control mechanism that must be considered when interpreting blood sodium.
- primary_references
- [sodium-p7532304] Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. (1995). https://pubmed.ncbi.nlm.nih.gov/7532304/ DOI: 10.1073/pnas.92.4.1013
- tissue_or_cell_type
- Inner medullary collecting duct
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 434–445
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy · source_derived_draft · unverified_draft
### sodium-avp-water Water permeability rose during vasopressin exposure and fell after withdrawal in parallel with AQP2 redistribution. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This is a water-control mechanism that must be considered when interpreting blood sodium. organism: Rat tissue_or_cell_type: Inner medullary collecting duct experimental_model: Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy limitations: Direct water-channel trafficking experiment; no claim that sodium dietary deficiency caused the response. exposure: Vasopressin addition and withdrawal evidence_span: {"source_cache": "artifacts/sodium-research/7532304.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4", "start_char": 0, "end_char": 1588, "text_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4"} [sodium-p7532304] Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. (1995). https://pubmed.ncbi.nlm.nih.gov/7532304/ DOI: 10.1073/pnas.92.4.1013
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.