Component

Aldosterone

Mineralocorticoid steroid hormone; plasma abundance is not interchangeable with ENaC activity.

10 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. Aldosterone increased collecting-duct sgk mRNA within 30 minutes through mineralocorticoid receptors without requiring new protein synthesis.

    Aldosterone → SGK1 transcript and protein expression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"}
    experimental_model
    Immediate-early gene induction and channel coexpression
    exposure
    Aldosterone exposure; receptor dependence and protein-synthesis tests
    limitations
    Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes
    plain_language
    A hormone can quickly increase the instructions for a kinase that regulates sodium transport.
    primary_references
    [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
    tissue_or_cell_type
    Cortical collecting duct and expression system

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 395–406

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Immediate-early gene induction and channel coexpression · source_derived_draft · unverified_draft

    ### sodium-aldosterone-sgk Aldosterone increased collecting-duct sgk mRNA within 30 minutes through mineralocorticoid receptors without requiring new protein synthesis. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A hormone can quickly increase the instructions for a kinase that regulates sodium transport. organism: Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes tissue_or_cell_type: Cortical collecting duct and expression system experimental_model: Immediate-early gene induction and channel coexpression limitations: Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue. exposure: Aldosterone exposure; receptor dependence and protein-synthesis tests evidence_span: {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"} [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
    Complete structured claim and evidence

What acts on it

  1. Plasma aldosterone in combined Na/Mg-restricted mice was not higher than with normal diet, although sodium restriction alone increased it.

    Magnesium → Aldosterone source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    magnesium -> sodium -> potassium
    experimental_model
    Dietary restriction in C57BL/6J mice with renal transport assays
    limitations
    Unchanged concentration does not imply absent mineralocorticoid action or exclude other ENaC regulators.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mus musculus
    plain_language
    The potassium loss pattern did not require a measured rise in circulating aldosterone in this experiment.
    primary_references
    [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
    tissue_or_cell_type
    Kidney distal nephron
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 191–201

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary restriction in C57BL/6J mice with renal transport assays · source_derived_draft · unverified_draft

    ### combined-na-mg-restriction-aldosterone-not-elevated Plasma aldosterone in combined Na/Mg-restricted mice was not higher than with normal diet, although sodium restriction alone increased it. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The potassium loss pattern did not require a measured rise in circulating aldosterone in this experiment. organism: Mus musculus tissue_or_cell_type: Kidney distal nephron experimental_model: Dietary restriction in C57BL/6J mice with renal transport assays limitations: Unchanged concentration does not imply absent mineralocorticoid action or exclude other ENaC regulators. cross_nutrient: magnesium -> sodium -> potassium [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
    Complete structured claim and evidence

  2. Intestinal NHE3-null mice had markedly elevated plasma aldosterone.

    Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Aldosterone source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"}
    experimental_model
    Inducible intestinal epithelial Slc9a3 deletion
    exposure
    Tamoxifen-induced NHE3 loss
    limitations
    Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    A strong hormonal conservation response did not prevent the phenotype.
    primary_references
    [sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
    tissue_or_cell_type
    Intestine with systemic electrolyte measurements
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 876–887

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible intestinal epithelial Slc9a3 deletion · source_derived_draft · unverified_draft

    ### sodium-gut-aldosterone Intestinal NHE3-null mice had markedly elevated plasma aldosterone. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A strong hormonal conservation response did not prevent the phenotype. organism: Mouse tissue_or_cell_type: Intestine with systemic electrolyte measurements experimental_model: Inducible intestinal epithelial Slc9a3 deletion limitations: Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion. exposure: Tamoxifen-induced NHE3 loss evidence_span: {"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"} [sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone.

    Potassium → Bicarbonate ion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Potassium and aldosterone-dependent sodium/acid handling jointly influence systemic bicarbonate.
    endpoint
    In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone.
    experimental-exposure
    Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement.
    experimental_model
    Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement.
    limitations
    Endocrine replacement experiment, not ordinary dietary deficiency; H/K-ATPase and H-ATPase were regulated differently.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rattus norvegicus
    plain_language
    Potassium depletion and mineralocorticoid exposure can act together on renal acid handling.
    primary_references
    [eiam-1993-atpases] Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium (1993). https://pubmed.ncbi.nlm.nih.gov/8390478/ DOI: 10.1172/JCI116471
    tissue_or_cell_type
    collecting tubule and systemic blood
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1137–1149

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement. · source_derived_draft · unverified_draft

    ### k-aldosterone-joint-bicarbonate In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium depletion and mineralocorticoid exposure can act together on renal acid handling. organism: Rattus norvegicus tissue_or_cell_type: collecting tubule and systemic blood experimental_model: Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement. limitations: Endocrine replacement experiment, not ordinary dietary deficiency; H/K-ATPase and H-ATPase were regulated differently. cross_nutrient: Potassium and aldosterone-dependent sodium/acid handling jointly influence systemic bicarbonate. experimental-exposure: Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement. endpoint: In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone. [eiam-1993-atpases] Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium (1993). https://pubmed.ncbi.nlm.nih.gov/8390478/ DOI: 10.1172/JCI116471
    Complete structured claim and evidence

  2. Potassium increased aldosterone, renin and copeptin in the post-hoc hormone analysis while blood pressure fell.

    Potassium → Plasma aldosterone concentration source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Potassium -> endocrine regulation; sodium/volume context retained.
    experimental_model
    35 participants from the same feeding trial.
    limitations
    Post-hoc circulating markers do not identify receptor signaling or a universal endocrine response.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens
    plain_language
    A hormone response can accompany a pressure reduction rather than imply the opposite outcome.
    primary_references
    [k-gijsbers2016-hormones] Effects of potassium supplementation on markers of osmoregulation and volume regulation: results of a fully controlled dietary intervention study (2016). https://pubmed.ncbi.nlm.nih.gov/26599222/ DOI: 10.1097/hjh.0000000000000786
    tissue_or_cell_type
    Plasma

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1568–1578

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 35 participants from the same feeding trial. · source_derived_draft · unverified_draft

    ### k-controlled-feeding-regulatory-hormones Potassium increased aldosterone, renin and copeptin in the post-hoc hormone analysis while blood pressure fell. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A hormone response can accompany a pressure reduction rather than imply the opposite outcome. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: 35 participants from the same feeding trial. limitations: Post-hoc circulating markers do not identify receptor signaling or a universal endocrine response. cross_nutrient: Potassium -> endocrine regulation; sodium/volume context retained. [k-gijsbers2016-hormones] Effects of potassium supplementation on markers of osmoregulation and volume regulation: results of a fully controlled dietary intervention study (2016). https://pubmed.ncbi.nlm.nih.gov/26599222/ DOI: 10.1097/hjh.0000000000000786
    Complete structured claim and evidence

  3. A potassium-containing meal increased K excretion without a detected serum K rise in the human study; the response persisted with eplerenone.

    Potassium → Urinary potassium excretion source_derived_draftungraded
    Experimental context and source evidence
    evidence_location
    Primary abstract; meal-plus-K and eplerenone comparisons.
    experimental_model
    Controlled meal challenges and MR-blockade comparison; 32 participants
    limitations
    Low-sodium controlled background; no gut receptor identified and complete aldosterone independence is an inference.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens
    plain_language
    People can increase potassium excretion after a meal before a measurable blood rise.
    primary_references
    [preston-2015-gut-human] Evidence for a gastrointestinal-renal kaliuretic signaling axis in humans (2015). https://pubmed.ncbi.nlm.nih.gov/26308672/ DOI: 10.1038/ki.2015.243
    tissue_or_cell_type
    Gastrointestinal-renal axis

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 472–482

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled meal challenges and MR-blockade comparison; 32 participants · source_derived_draft · unverified_draft

    ### renal-human-meal-k-excretion-without-serum-rise A potassium-containing meal increased K excretion without a detected serum K rise in the human study; the response persisted with eplerenone. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: People can increase potassium excretion after a meal before a measurable blood rise. organism: Homo sapiens tissue_or_cell_type: Gastrointestinal-renal axis experimental_model: Controlled meal challenges and MR-blockade comparison; 32 participants limitations: Low-sodium controlled background; no gut receptor identified and complete aldosterone independence is an inference. evidence_location: Primary abstract; meal-plus-K and eplerenone comparisons. [preston-2015-gut-human] Evidence for a gastrointestinal-renal kaliuretic signaling axis in humans (2015). https://pubmed.ncbi.nlm.nih.gov/26308672/ DOI: 10.1038/ki.2015.243
    Complete structured claim and evidence

  4. Nephron-wide MR deletion impaired apical ENaC orientation/cleavage and produced hyperkalemia with salt wasting in adult mice.

    Mineralocorticoid receptor → ENaC proteolytic processing source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Defective sodium-channel regulation compromises K balance.
    evidence_location
    Abstract; Results Figures 1 and 5.
    experimental_model
    Inducible renal MR deletion
    limitations
    NCC remained activatable by K restriction; receptor effects on NCC are not assumed to be direct.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mus musculus
    plain_language
    The mineralocorticoid receptor helps maintain the sodium-channel machinery needed for normal potassium balance.
    primary_references
    [terker-2016-mineralocorticoid] Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4978056/ DOI: 10.1681/ASN.2015070815
    tissue_or_cell_type
    Aldosterone-sensitive distal nephron
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 395–406

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible renal MR deletion · source_derived_draft · unverified_draft

    ### renal-mr-supports-enac-processing Nephron-wide MR deletion impaired apical ENaC orientation/cleavage and produced hyperkalemia with salt wasting in adult mice. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mineralocorticoid receptor helps maintain the sodium-channel machinery needed for normal potassium balance. organism: Mus musculus tissue_or_cell_type: Aldosterone-sensitive distal nephron experimental_model: Inducible renal MR deletion limitations: NCC remained activatable by K restriction; receptor effects on NCC are not assumed to be direct. cross_nutrient: Defective sodium-channel regulation compromises K balance. evidence_location: Abstract; Results Figures 1 and 5. [terker-2016-mineralocorticoid] Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4978056/ DOI: 10.1681/ASN.2015070815
    Complete structured claim and evidence

  5. Oral K rapidly dephosphorylated NCC in mice, including aldosterone-deficient animals.

    Potassium → NCC phosphorylation source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    K loading suppresses a Na/Cl transporter before some hormonal adaptations.
    evidence_location
    Primary abstract; early NCC time course and aldosterone-deficient mice.
    experimental_model
    Gastric K load; aldosterone-deficient comparison
    limitations
    Early response differs from later ENaC activation; acute gavage is not a chronic diet.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mus musculus
    plain_language
    The earliest NCC response to potassium does not require a new aldosterone signal in this model.
    primary_references
    [sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14
    tissue_or_cell_type
    Kidney DCT

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 294–305

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gastric K load; aldosterone-deficient comparison · source_derived_draft · unverified_draft

    ### renal-oral-k-aldosterone-independent-ncc-off Oral K rapidly dephosphorylated NCC in mice, including aldosterone-deficient animals. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The earliest NCC response to potassium does not require a new aldosterone signal in this model. organism: Mus musculus tissue_or_cell_type: Kidney DCT experimental_model: Gastric K load; aldosterone-deficient comparison limitations: Early response differs from later ENaC activation; acute gavage is not a chronic diet. cross_nutrient: K loading suppresses a Na/Cl transporter before some hormonal adaptations. evidence_location: Primary abstract; early NCC time course and aldosterone-deficient mice. [sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14
    Complete structured claim and evidence

  6. Potassium-containing meals produced more renal K excretion than K-free meals plus intravenous KCl despite matched plasma K profiles in rats.

    Potassium → Urinary potassium excretion source_derived_draftungraded
    Experimental context and source evidence
    evidence_location
    Study 1 and primary abstract.
    experimental_model
    Meal comparison with plasma-profile-matched KCl infusion
    limitations
    The responsible sensor/factor was unidentified; matching sampled plasma does not exclude every local signal.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rattus norvegicus
    plain_language
    The meal-associated signal adds to the effect of potassium measured in blood.
    primary_references
    [oh-2011-gut-k] Gut sensing of dietary K+ intake increases renal K+ excretion (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3154709/ DOI: 10.1152/ajpregu.00095.2011
    tissue_or_cell_type
    Gastrointestinal-renal axis

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 460–470

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Meal comparison with plasma-profile-matched KCl infusion · source_derived_draft · unverified_draft

    ### renal-rat-meal-k-excretion-beyond-plasma Potassium-containing meals produced more renal K excretion than K-free meals plus intravenous KCl despite matched plasma K profiles in rats. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The meal-associated signal adds to the effect of potassium measured in blood. organism: Rattus norvegicus tissue_or_cell_type: Gastrointestinal-renal axis experimental_model: Meal comparison with plasma-profile-matched KCl infusion limitations: The responsible sensor/factor was unidentified; matching sampled plasma does not exclude every local signal. evidence_location: Study 1 and primary abstract. [oh-2011-gut-k] Gut sensing of dietary K+ intake increases renal K+ excretion (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3154709/ DOI: 10.1152/ajpregu.00095.2011
    Complete structured claim and evidence

  7. Immersion at thermoneutral 32 degrees C did not change rectal temperature or metabolic rate but lowered heart rate by 15% and blood pressure by 11 to 12%, lowered plasma renin activity by 46%, cortisol by 34% and aldosterone by 17%, and increased diuresis by 107%.

    Hydrostatic pressure of head-out water immersion, separate from its temperature → Urine output / diuresis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/cold-research/10751106.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d018fda7c67dc61bb0d4a38ddfd7850e7252897587c5a4477607271b10d42291", "start_char": 0, "end_char": 2332, "text_sha256": "d018fda7c67dc61bb0d4a38ddfd7850e7252897587c5a4477607271b10d42291"}
    experimental_model
    Young men during 1-hour head-out immersions at 32, 20 and 14 degrees C
    exposure
    One hour head-out immersion at three water temperatures
    limitations
    The thermoneutral arm separates hydrostatic pressure from cold. Cortisol did not rise at any temperature, which bears directly on calling immersion a stress response.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Human
    plain_language
    Simply being in water, at any temperature, drops blood pressure and makes you urinate.
    primary_references
    [cold-p10751106] Human physiological responses to immersion into water of different temperatures. (2000). https://pubmed.ncbi.nlm.nih.gov/10751106/ DOI: 10.1007/s004210050065
    tissue_or_cell_type
    Whole body

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 169–180

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Young men during 1-hour head-out immersions at 32, 20 and 14 degrees C · source_derived_draft · unverified_draft

    ### cold-pressure-versus-cold Immersion at thermoneutral 32 degrees C did not change rectal temperature or metabolic rate but lowered heart rate by 15% and blood pressure by 11 to 12%, lowered plasma renin activity by 46%, cortisol by 34% and aldosterone by 17%, and increased diuresis by 107%. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Simply being in water, at any temperature, drops blood pressure and makes you urinate. organism: Human tissue_or_cell_type: Whole body experimental_model: Young men during 1-hour head-out immersions at 32, 20 and 14 degrees C limitations: The thermoneutral arm separates hydrostatic pressure from cold. Cortisol did not rise at any temperature, which bears directly on calling immersion a stress response. exposure: One hour head-out immersion at three water temperatures evidence_span: {"source_cache": "artifacts/cold-research/10751106.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d018fda7c67dc61bb0d4a38ddfd7850e7252897587c5a4477607271b10d42291", "start_char": 0, "end_char": 2332, "text_sha256": "d018fda7c67dc61bb0d4a38ddfd7850e7252897587c5a4477607271b10d42291"} [cold-p10751106] Human physiological responses to immersion into water of different temperatures. (2000). https://pubmed.ncbi.nlm.nih.gov/10751106/ DOI: 10.1007/s004210050065
    Complete structured claim and evidence

In the sources

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