Component
Mouse endothelial nitric oxide synthase / Nos3
Mouse endothelial nitric oxide synthase / Nos3
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Thalamic microvessel endothelial NOS immunoreactivity increased after ten days of the mouse depletion protocol.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_location
- Results: NOS Induction; Figure 3
- evidence_span
- enhanced endothelial NOS immunoreactivity
- experimental_model
- Adult male C57BL/6 mice and Fischer 344 Brown Norway F1 rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day intraperitoneally; staged brain histochemistry.
- exposure
- Dietary thiamine removal plus daily pyrithiamine in mice or rats
- limitations
- Immunostaining is not a direct nitric oxide flux measurement and does not establish a protective or damaging net effect.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Mus musculus
- plain_language
- The blood-vessel lining increased its endothelial nitric oxide synthase signal.
- primary_references
- [calingasan-1998-bbb-iron-nos] Induction of nitric oxide synthase and microglial responses precede selective cell death induced by chronic impairment of oxidative metabolism (1998). https://pmc.ncbi.nlm.nih.gov/articles/PMC1852979/ DOI: 10.1016/S0002-9440(10)65602-7
- tissue_or_cell_type
- Thalamic microvessel walls
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1197–1209
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adult male C57BL/6 mice and Fischer 344 Brown Norway F1 rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day intraperitoneally; staged brain histochemistry. · source_derived_draft · unverified_draft
### thiamine-def-mouse-endothelial-nos3 Thalamic microvessel endothelial NOS immunoreactivity increased after ten days of the mouse depletion protocol. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The blood-vessel lining increased its endothelial nitric oxide synthase signal. organism: Mus musculus tissue_or_cell_type: Thalamic microvessel walls experimental_model: Adult male C57BL/6 mice and Fischer 344 Brown Norway F1 rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day intraperitoneally; staged brain histochemistry. limitations: Immunostaining is not a direct nitric oxide flux measurement and does not establish a protective or damaging net effect. evidence_location: Results: NOS Induction; Figure 3 evidence_span: enhanced endothelial NOS immunoreactivity exposure: Dietary thiamine removal plus daily pyrithiamine in mice or rats [calingasan-1998-bbb-iron-nos] Induction of nitric oxide synthase and microglial responses precede selective cell death induced by chronic impairment of oxidative metabolism (1998). https://pmc.ncbi.nlm.nih.gov/articles/PMC1852979/ DOI: 10.1016/S0002-9440(10)65602-7
Complete structured claim and evidence
Where it participates (unsigned role)
BH4 oxidation accompanied eNOS uncoupling with increased ROS and reduced NO in hypertensive mouse aortas.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/citrulline-research/12697739.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d56604695c8c1bda167b76198a472d814d284a3c0c1e1e1eed8943cce31d0ad0", "start_char": 0, "end_char": 1474, "text_sha256": "d56604695c8c1bda167b76198a472d814d284a3c0c1e1e1eed8943cce31d0ad0"}
- experimental_model
- Hypertension and knockout mouse experiments
- exposure
- NADPH-oxidase/NOS genetic comparisons and BH4 treatment
- limitations
- Disease model; the exact response cannot be assumed in people taking citrulline.
- nutrient_topic
- Citrulline research collection; topical membership is not evidence of a direct dietary effect. · L-Citrulline
- organism
- Mouse DOCA-salt hypertension model
- plain_language
- Adding precursor is different from fixing a damaged cofactor system.
- primary_references
- [citrulline-p12697739] Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension. (2003). https://pubmed.ncbi.nlm.nih.gov/12697739/ DOI: 10.1172/jci14172
- tissue_or_cell_type
- Aortic redox state and NO signaling
Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 801–812
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hypertension and knockout mouse experiments · source_derived_draft · unverified_draft
### citrulline-bh4-oxidation BH4 oxidation accompanied eNOS uncoupling with increased ROS and reduced NO in hypertensive mouse aortas. Condition category: normal nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding precursor is different from fixing a damaged cofactor system. organism: Mouse DOCA-salt hypertension model tissue_or_cell_type: Aortic redox state and NO signaling experimental_model: Hypertension and knockout mouse experiments limitations: Disease model; the exact response cannot be assumed in people taking citrulline. exposure: NADPH-oxidase/NOS genetic comparisons and BH4 treatment evidence_span: {"source_cache": "artifacts/citrulline-research/12697739.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d56604695c8c1bda167b76198a472d814d284a3c0c1e1e1eed8943cce31d0ad0", "start_char": 0, "end_char": 1474, "text_sha256": "d56604695c8c1bda167b76198a472d814d284a3c0c1e1e1eed8943cce31d0ad0"} [citrulline-p12697739] Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension. (2003). https://pubmed.ncbi.nlm.nih.gov/12697739/ DOI: 10.1172/jci14172
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.