Component

Mouse sodium/hydrogen exchanger NHE3 / Slc9a3

Mouse sodium/hydrogen exchanger NHE3 / Slc9a3. Species, exposure and limitations are retained in each linked claim.

9 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. 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

  2. Intestinal NHE3-null mice developed metabolic acidosis with lower blood bicarbonate.

    Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Plasma bicarbonate concentration 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
    The losses also disturbed acid–base balance.
    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 837–848

    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-bicarbonate Intestinal NHE3-null mice developed metabolic acidosis with lower blood bicarbonate. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The losses also disturbed acid–base balance. 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

  3. Intestinal NHE3 deletion produced persistent watery, alkaline diarrhea.

    Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Intestinal fluid loss 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 transport defect can create ongoing intestinal fluid losses.
    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 824–835

    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-loss Intestinal NHE3 deletion produced persistent watery, alkaline diarrhea. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transport defect can create ongoing intestinal fluid losses. 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

  4. Intestinal NHE3-null mice developed hyperkalemia.

    Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Plasma potassium concentration 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
    Potassium can rise in this model; diarrhea does not impose one universal potassium pattern.
    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 863–874

    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-potassium Intestinal NHE3-null mice developed hyperkalemia. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium can rise in this model; diarrhea does not impose one universal potassium pattern. 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

  5. Intestinal NHE3-null mice developed hyponatremia.

    Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Plasma or serum sodium concentration 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 gut transport defect can affect the measured blood sodium.
    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 850–861

    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-sodium Intestinal NHE3-null mice developed hyponatremia. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A gut transport defect can affect the measured blood sodium. 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

  6. Kidney-specific NHE3 deletion did not change the measured baseline plasma sodium, pH or bicarbonate.

    Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Plasma or serum sodium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"}
    experimental_model
    Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes
    exposure
    Genetic deletion; increased perfusion pressure; saline and dietary salt challenges
    limitations
    Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    Changed sodium handling need not produce a changed blood sodium value.
    primary_references
    [sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
    tissue_or_cell_type
    Kidney proximal tubule
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 915–926

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes · source_derived_draft · unverified_draft

    ### sodium-renal-nhe3-marker Kidney-specific NHE3 deletion did not change the measured baseline plasma sodium, pH or bicarbonate. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changed sodium handling need not produce a changed blood sodium value. organism: Mouse tissue_or_cell_type: Kidney proximal tubule experimental_model: Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes limitations: Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction. exposure: Genetic deletion; increased perfusion pressure; saline and dietary salt challenges evidence_span: {"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"} [sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
    Complete structured claim and evidence

  7. A 30-mmHg perfusion-pressure increase raised sodium excretion fivefold in controls and eightfold in proximal NHE3-null mice.

    Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Urinary sodium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"}
    experimental_model
    Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes
    exposure
    Genetic deletion; increased perfusion pressure; saline and dietary salt challenges
    limitations
    Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    The kidney excreted more sodium in response to pressure when this reabsorption route was missing.
    primary_references
    [sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
    tissue_or_cell_type
    Kidney proximal tubule
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 889–900

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes · source_derived_draft · unverified_draft

    ### sodium-renal-nhe3-natriuresis A 30-mmHg perfusion-pressure increase raised sodium excretion fivefold in controls and eightfold in proximal NHE3-null mice. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney excreted more sodium in response to pressure when this reabsorption route was missing. organism: Mouse tissue_or_cell_type: Kidney proximal tubule experimental_model: Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes limitations: Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction. exposure: Genetic deletion; increased perfusion pressure; saline and dietary salt challenges evidence_span: {"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"} [sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
    Complete structured claim and evidence

  8. Proximal-tubule NHE3-null mice had lower basal systolic, diastolic and mean arterial pressure.

    Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Arterial blood pressure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"}
    experimental_model
    Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes
    exposure
    Genetic deletion; increased perfusion pressure; saline and dietary salt challenges
    limitations
    Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    A kidney sodium-transport change can affect blood pressure.
    primary_references
    [sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
    tissue_or_cell_type
    Kidney proximal tubule
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 902–913

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes · source_derived_draft · unverified_draft

    ### sodium-renal-nhe3-pressure Proximal-tubule NHE3-null mice had lower basal systolic, diastolic and mean arterial pressure. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A kidney sodium-transport change can affect blood pressure. organism: Mouse tissue_or_cell_type: Kidney proximal tubule experimental_model: Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes limitations: Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction. exposure: Genetic deletion; increased perfusion pressure; saline and dietary salt challenges evidence_span: {"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"} [sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
    Complete structured claim and evidence

What acts on it

  1. NHE3 also redistributed toward intracellular vesicles at steady state despite slower internalization.

    Mouse ClC-5 chloride/proton exchanger / Clcn5 → Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chloride-research/11099045.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca", "start_char": 0, "end_char": 1218, "text_sha256": "4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca"}
    experimental_model
    Clcn5 knockout and uptake measurements
    exposure
    Clcn5 disruption
    limitations
    The PTH/vitamin-D/hypercalciuria explanation includes proposed downstream steps; do not treat every link as demonstrated.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse
    plain_language
    The sodium/hydrogen exchanger changed location too.
    primary_references
    [chloride-p11099045] ClC-5 Cl- -channel disruption impairs endocytosis in a mouse model for Dent's disease. (2000). https://pubmed.ncbi.nlm.nih.gov/11099045/ DOI: 10.1038/35042597
    tissue_or_cell_type
    Proximal renal tubule
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 731–742

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clcn5 knockout and uptake measurements · source_derived_draft · unverified_draft

    ### chloride-clc5-nhe3 NHE3 also redistributed toward intracellular vesicles at steady state despite slower internalization. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: The sodium/hydrogen exchanger changed location too. organism: Mouse tissue_or_cell_type: Proximal renal tubule experimental_model: Clcn5 knockout and uptake measurements limitations: The PTH/vitamin-D/hypercalciuria explanation includes proposed downstream steps; do not treat every link as demonstrated. exposure: Clcn5 disruption evidence_span: {"source_cache": "artifacts/chloride-research/11099045.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca", "start_char": 0, "end_char": 1218, "text_sha256": "4929ed9da0f3702bbd28bf679f79c2dfb13b4e81d23e44327b27bebdcf3a7cca"} [chloride-p11099045] ClC-5 Cl- -channel disruption impairs endocytosis in a mouse model for Dent's disease. (2000). https://pubmed.ncbi.nlm.nih.gov/11099045/ DOI: 10.1038/35042597
    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