{"id":"4fe573f9-ea42-519f-83ed-747815e62b49","stable_key":"5102beb6-9f61-500e-af10-9ac63649e0b7:renal-ncc-loss-blunts-k-natriuresis","predicate":"contributes-to-potassium-induced","statement":"NCC-deficient mice showed markedly less sodium excretion after the acute oral K load than controls.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"positive","is_public":true,"mechanism_event_id":"38151f9d-7711-5f0a-9121-6f5de7a215dc","mechanism_event_label":"Turning NCC down contributes to the sodium loss caused by potassium loading.","subject":{"id":"63291643-1df9-5547-952a-9082838a350e","slug":"slc12a3","display_name":"Thiazide-sensitive sodium-chloride cotransporter","entity_type_key":"protein"},"object":{"id":"fd3a60b1-8952-526a-b67b-10923acd61b1","slug":"urinary-sodium-excretion","display_name":"Urinary sodium excretion","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"38151f9d-7711-5f0a-9121-6f5de7a215dc","stable_key":"5102beb6-9f61-500e-af10-9ac63649e0b7:renal-ncc-loss-blunts-k-natriuresis-event","event_type":"biochemical_relationship","label":"Turning NCC down contributes to the sodium loss caused by potassium loading.","description":"NCC-deficient mice showed markedly less sodium excretion after the acute oral K load than controls.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"63291643-1df9-5547-952a-9082838a350e","slug":"slc12a3","display_name":"Thiazide-sensitive sodium-chloride cotransporter","entity_type_key":"protein"},"role":"causal-subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"fd3a60b1-8952-526a-b67b-10923acd61b1","slug":"urinary-sodium-excretion","display_name":"Urinary sodium excretion","entity_type_key":"cellular_process"},"role":"measured-target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"87435e1d-e1cd-57da-984b-203b2f5f29a4","slug":"potassium","display_name":"Potassium","entity_type_key":"nutrient_element"},"role":"oral-exposure","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"38de8704-84db-5770-ac1d-242cd787e798","slug":"sodium-ion","display_name":"Sodium ion","entity_type_key":"ion"},"role":"excreted-ion","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""},{"entity":{"id":"8197e69c-215b-5cd4-bf4b-edde6708ea8f","slug":"ncc-phosphorylation","display_name":"NCC phosphorylation","entity_type_key":"cellular_process"},"role":"related-readout","stoichiometry":null,"state_label":"","sequence_order":4,"notes":""}]},"contexts":[{"dimension":"cross_nutrient","value_text":"K loading can increase sodium excretion through NCC regulation.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"evidence_location","value_text":"Primary abstract; NCC-deficient natriuresis comparison.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"NCC knockout and control K gavage","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"This does not establish that increased distal sodium delivery alone explains all kaliuresis.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Potassium research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"potassium","display_name":"Potassium","entity_type_key":"nutrient_element"}},{"dimension":"organism","value_text":"Mus musculus","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"Turning NCC down contributes to the sodium loss caused by potassium loading.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[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","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Kidney","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"bf7b17d1-177f-5537-b682-82e2d5de904f","evidence_kind":"source_excerpt","locator":"Lines 307-318","start_line":307,"end_line":318,"excerpt":"### renal-ncc-loss-blunts-k-natriuresis\nNCC-deficient mice showed markedly less sodium excretion after the acute oral K load than controls.\nCondition category: normal\nnutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Turning NCC down contributes to the sodium loss caused by potassium loading.\norganism: Mus musculus\ntissue_or_cell_type: Kidney\nexperimental_model: NCC knockout and control K gavage\nlimitations: This does not establish that increased distal sodium delivery alone explains all kaliuresis.\ncross_nutrient: K loading can increase sodium excretion through NCC regulation.\nevidence_location: Primary abstract; NCC-deficient natriuresis comparison.\n[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","model_system":"NCC knockout and control K gavage","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study 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","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"241226ee-6b7d-5cc7-9781-e6beb8ee1982","stable_key":"import-5102beb6-9f61-500e-af10-9ac63649e0b7","title":"Potassium: cross-nutrient mechanisms and deficiency (2026-09-17)","document_type":"imported_text","citation_label":"AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text.","file_path":"","sha256":"a8f89f8d84b48c0f93048dfc45f7f57a67dd9a7249968a096a14aeb03d8b7a52","revision_id":"de4ec6f4-58a1-537b-8169-97b783898df1","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}