Component

Arginine vasopressin / antidiuretic hormone

Arginine vasopressin / antidiuretic hormone. Species, exposure and limitations are retained in each linked claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Vasopressin increased apical AQP2 labeling and shifted AQP2 from intracellular vesicles toward the apical membrane.

    Arginine vasopressin / antidiuretic hormone → Apical collecting-duct aquaporin-2 abundance source_derived_draftungraded
    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 evidence

  2. Water permeability rose during vasopressin exposure and fell after withdrawal in parallel with AQP2 redistribution.

    Arginine vasopressin / antidiuretic hormone → Collecting-duct osmotic water permeability source_derived_draftungraded
    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

Where it participates (unsigned role)

  1. Vasodilatory renal prostaglandins are relatively unimportant under normal circumstances but play a modulatory role after ischaemia or in the presence of increased concentrations of vasoconstrictor substances such as angiotensin II, vasopressin or norepinephrine, indomethacin potentiates the renal actions of angiotensin II in vivo particularly the reduction of renal blood flow and filtration rate, and in dogs after chronic bile duct ligation cyclooxygenase inhibition by indomethacin, ibuprofen, naproxen or sulindac sulfide produced a comparable 50% decrease in both renal blood flow and filtration rate.

    The vasodilatory prostaglandin reserve that supports renal blood flow under stress → Glomerular filtration rate measured by creatinine clearance source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ibuprofen-research/6595999.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cf73667739f04e5edcaf0e75c1f413cbda7abbfe84b8701b1aeaa347b67809c2", "start_char": 0, "end_char": 2422, "text_sha256": "cf73667739f04e5edcaf0e75c1f413cbda7abbfe84b8701b1aeaa347b67809c2"}
    experimental_model
    Review of renal cortical prostaglandin physiology with dog bile duct ligation and human volunteer data
    exposure
    Cyclooxygenase inhibition against a background of raised vasoconstrictor tone
    limitations
    A review assembling several models rather than one experiment. It states the conditional nature of the renal prostaglandin role, which is the point recorded here.
    nutrient_topic
    Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
    organism
    Rat, dog and human
    plain_language
    These prostaglandins are a reserve the kidney calls on under strain, which is why blocking them is harmless until it is not.
    primary_references
    [ibu-p6595999] Mechanisms of the nephrotoxicity of non-steroidal anti-inflammatory drugs. (1984). https://pubmed.ncbi.nlm.nih.gov/6595999/ DOI: 10.1007/978-3-642-69132-4_56
    tissue_or_cell_type
    Renal cortex and glomeruli

    Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 474–485

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of renal cortical prostaglandin physiology with dog bile duct ligation and human volunteer data · source_derived_draft · unverified_draft

    ### ibu-a-reserve-not-a-baseline Vasodilatory renal prostaglandins are relatively unimportant under normal circumstances but play a modulatory role after ischaemia or in the presence of increased concentrations of vasoconstrictor substances such as angiotensin II, vasopressin or norepinephrine, indomethacin potentiates the renal actions of angiotensin II in vivo particularly the reduction of renal blood flow and filtration rate, and in dogs after chronic bile duct ligation cyclooxygenase inhibition by indomethacin, ibuprofen, naproxen or sulindac sulfide produced a comparable 50% decrease in both renal blood flow and filtration rate. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: These prostaglandins are a reserve the kidney calls on under strain, which is why blocking them is harmless until it is not. organism: Rat, dog and human tissue_or_cell_type: Renal cortex and glomeruli experimental_model: Review of renal cortical prostaglandin physiology with dog bile duct ligation and human volunteer data limitations: A review assembling several models rather than one experiment. It states the conditional nature of the renal prostaglandin role, which is the point recorded here. exposure: Cyclooxygenase inhibition against a background of raised vasoconstrictor tone evidence_span: {"source_cache": "artifacts/ibuprofen-research/6595999.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cf73667739f04e5edcaf0e75c1f413cbda7abbfe84b8701b1aeaa347b67809c2", "start_char": 0, "end_char": 2422, "text_sha256": "cf73667739f04e5edcaf0e75c1f413cbda7abbfe84b8701b1aeaa347b67809c2"} [ibu-p6595999] Mechanisms of the nephrotoxicity of non-steroidal anti-inflammatory drugs. (1984). https://pubmed.ncbi.nlm.nih.gov/6595999/ DOI: 10.1007/978-3-642-69132-4_56
    Complete structured claim and evidence

  2. Hypothalamic TRPV1 expression, hypothalamic intracellular calcium concentration and arginine vasopressin concentration in the ventral septum were significantly higher in the dihydrocapsaicin group than in the control, resuscitation and body surface cooling groups, and the authors concluded that dihydrocapsaicin activates TRPV1 on hypothalamic cells to cause a large calcium influx which causes the release of vasopressin to induce hypothermia.

    Dihydrocapsaicin → Calcium influx into hypothalamic cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/29035676.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98", "start_char": 0, "end_char": 2035, "text_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98"}
    experimental_model
    Four-group asphyxia arrest study in 24 male Sprague Dawley rats with immunohistochemistry and tissue assays
    exposure
    Dihydrocapsaicin against cardiopulmonary resuscitation alone and against body surface cooling
    limitations
    Proposes the central mechanism and measures each step, but with six animals per group and immunohistochemical rather than functional readouts.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Rat
    plain_language
    The proposed route runs through the brain’s thermostat: calcium floods in and a hormone is released.
    primary_references
    [dhc-p29035676] The Molecular Mechanism and Neuroprotective Effect of Dihydrocapsaicin-Induced Mild Hypothermia After Cardiopulmonary Resuscitation in Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29035676/ DOI: 10.1089/ther.2017.0032
    tissue_or_cell_type
    Hypothalamus, ventral septum and cerebral cortex

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 426–437

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-group asphyxia arrest study in 24 male Sprague Dawley rats with immunohistochemistry and tissue assays · source_derived_draft · unverified_draft

    ### dhc-hypothalamic-calcium-avp Hypothalamic TRPV1 expression, hypothalamic intracellular calcium concentration and arginine vasopressin concentration in the ventral septum were significantly higher in the dihydrocapsaicin group than in the control, resuscitation and body surface cooling groups, and the authors concluded that dihydrocapsaicin activates TRPV1 on hypothalamic cells to cause a large calcium influx which causes the release of vasopressin to induce hypothermia. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: The proposed route runs through the brain’s thermostat: calcium floods in and a hormone is released. organism: Rat tissue_or_cell_type: Hypothalamus, ventral septum and cerebral cortex experimental_model: Four-group asphyxia arrest study in 24 male Sprague Dawley rats with immunohistochemistry and tissue assays limitations: Proposes the central mechanism and measures each step, but with six animals per group and immunohistochemical rather than functional readouts. exposure: Dihydrocapsaicin against cardiopulmonary resuscitation alone and against body surface cooling evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/29035676.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98", "start_char": 0, "end_char": 2035, "text_sha256": "bb8f6fadb6a90a5afbd08a767fde07137140f2bf8cc536207ca8619e4168bf98"} [dhc-p29035676] The Molecular Mechanism and Neuroprotective Effect of Dihydrocapsaicin-Induced Mild Hypothermia After Cardiopulmonary Resuscitation in Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29035676/ DOI: 10.1089/ther.2017.0032
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards