Component

Plasma bicarbonate concentration

Independent biological entity. Read linked claims for experimental scope and context.

5 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 acts on it

  1. 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

  2. Serum bicarbonate was 27.4 versus 24 meq/L in pendrin-null and control mice.

    Mouse pendrin / Slc26a4 → Plasma bicarbonate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/chloride-research/20375274.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953", "start_char": 0, "end_char": 1797, "text_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953"}
    experimental_model
    Pendrin knockout and isolated collecting-duct perfusion
    exposure
    Slc26a4 deletion
    limitations
    Residual exchange remained; baseline urine chloride excretion was unchanged.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Mouse
    plain_language
    A local transporter defect changed the blood acid–base measurement.
    primary_references
    [chloride-p20375274] Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl(-)/HCO3(-) exchanger activity and impairs bicarbonate secretion in kidney collecting duct. (2010). https://pubmed.ncbi.nlm.nih.gov/20375274/ DOI: 10.1152/ajpcell.00033.2010
    tissue_or_cell_type
    Non-acid-secreting intercalated cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 523–534

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pendrin knockout and isolated collecting-duct perfusion · source_derived_draft · unverified_draft

    ### chloride-pendrin-blood-bicarbonate Serum bicarbonate was 27.4 versus 24 meq/L in pendrin-null and control mice. Condition category: machinery_impairment nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: A local transporter defect changed the blood acid–base measurement. organism: Mouse tissue_or_cell_type: Non-acid-secreting intercalated cells experimental_model: Pendrin knockout and isolated collecting-duct perfusion limitations: Residual exchange remained; baseline urine chloride excretion was unchanged. exposure: Slc26a4 deletion evidence_span: {"source_cache": "artifacts/chloride-research/20375274.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953", "start_char": 0, "end_char": 1797, "text_sha256": "8ddda637993b80b24351aefe0451312d849175bd3ec2f3af23b72b50f7439953"} [chloride-p20375274] Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl(-)/HCO3(-) exchanger activity and impairs bicarbonate secretion in kidney collecting duct. (2010). https://pubmed.ncbi.nlm.nih.gov/20375274/ DOI: 10.1152/ajpcell.00033.2010
    Complete structured claim and evidence

  3. The same KCl load did not change acid–base status in sodium-depleted subjects who were not chloride-depleted.

    Potassium chloride → Plasma bicarbonate concentration source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chloride-research/2450456.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3df006f26c20c11aeb8fd26884ccbd5d1389921d34a40adad6f72edc184360d7", "start_char": 0, "end_char": 1348, "text_sha256": "3df006f26c20c11aeb8fd26884ccbd5d1389921d34a40adad6f72edc184360d7"}
    experimental_model
    Human depletion–repletion balance experiment
    exposure
    Furosemide plus restricted NaCl; oral KCl repletion over 36 hours
    limitations
    Loss-associated depletion; KCl supplies potassium too. Mechanism does not imply self-treatment or apply to every alkalosis.
    nutrient_topic
    Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
    organism
    Human men
    plain_language
    The response depended on chloride depletion, not merely on receiving KCl.
    primary_references
    [chloride-p2450456] On the mechanism by which chloride corrects metabolic alkalosis in man. (1988). https://pubmed.ncbi.nlm.nih.gov/2450456/ DOI: 10.1016/0002-9343(88)90265-3
    tissue_or_cell_type
    Kidney and systemic acid–base balance

    Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 861–872

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human depletion–repletion balance experiment · source_derived_draft · unverified_draft

    ### chloride-repletion-control The same KCl load did not change acid–base status in sodium-depleted subjects who were not chloride-depleted. Condition category: normal nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response depended on chloride depletion, not merely on receiving KCl. organism: Human men tissue_or_cell_type: Kidney and systemic acid–base balance experimental_model: Human depletion–repletion balance experiment limitations: Loss-associated depletion; KCl supplies potassium too. Mechanism does not imply self-treatment or apply to every alkalosis. exposure: Furosemide plus restricted NaCl; oral KCl repletion over 36 hours evidence_span: {"source_cache": "artifacts/chloride-research/2450456.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3df006f26c20c11aeb8fd26884ccbd5d1389921d34a40adad6f72edc184360d7", "start_char": 0, "end_char": 1348, "text_sha256": "3df006f26c20c11aeb8fd26884ccbd5d1389921d34a40adad6f72edc184360d7"} [chloride-p2450456] On the mechanism by which chloride corrects metabolic alkalosis in man. (1988). https://pubmed.ncbi.nlm.nih.gov/2450456/ DOI: 10.1016/0002-9343(88)90265-3
    Complete structured claim and evidence

  4. The same KCl run-in modestly lowered mean bicarbonate from 24.5 to 23.7 mmol/L and increased chloride; urinary ammonium did not increase.

    Potassium chloride → Plasma bicarbonate concentration source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Potassium salt/chloride -> acid-base balance.
    experimental_model
    Same two-week CKD cohort.
    limitations
    No randomized comparator; no significant blood-pressure or eGFR change.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens
    plain_language
    The chloride salt affected acid-base measurements as well as potassium.
    primary_references
    [k-gritter2022] Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD (2022). https://pubmed.ncbi.nlm.nih.gov/35609996/ DOI: 10.1681/asn.2022020147
    tissue_or_cell_type
    Plasma and urine

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1650–1660

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same two-week CKD cohort. · source_derived_draft · unverified_draft

    ### k-ckd-kcl-bicarbonate-response The same KCl run-in modestly lowered mean bicarbonate from 24.5 to 23.7 mmol/L and increased chloride; urinary ammonium did not increase. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The chloride salt affected acid-base measurements as well as potassium. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Same two-week CKD cohort. limitations: No randomized comparator; no significant blood-pressure or eGFR change. cross_nutrient: Potassium salt/chloride -> acid-base balance. [k-gritter2022] Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD (2022). https://pubmed.ncbi.nlm.nih.gov/35609996/ DOI: 10.1681/asn.2022020147
    Complete structured claim and evidence

  5. Bicarbonate salts and potassium gluconate increased bicarbonate in the CKD crossover; urinary citrate rose and ammonium fell.

    Potassium bicarbonate → Plasma bicarbonate concentration source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Salt anion -> bicarbonate/citrate/ammonium.
    experimental_model
    31 participants; five-day randomized periods.
    limitations
    Short exposure and washout; unchanged diet advised rather than controlled.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens
    plain_language
    The accompanying anion changed the acid-base response.
    primary_references
    [k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
    tissue_or_cell_type
    Plasma and urine

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1662–1672

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 31 participants; five-day randomized periods. · source_derived_draft · unverified_draft

    ### k-ckd-salts-alkalizing-comparison Bicarbonate salts and potassium gluconate increased bicarbonate in the CKD crossover; urinary citrate rose and ammonium fell. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The accompanying anion changed the acid-base response. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: 31 participants; five-day randomized periods. limitations: Short exposure and washout; unchanged diet advised rather than controlled. cross_nutrient: Salt anion -> bicarbonate/citrate/ammonium. [k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
    Complete structured claim and evidence

In the sources

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

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