Component
RhoA and Rho-kinase-mediated calcium sensitisation of contraction
RhoA and Rho-kinase-mediated calcium sensitisation of contraction. Species, exposure and limitations are retained in each linked claim.
1 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
Chronic hypoxia decreased RhoA messenger RNA and protein expression in rat main pulmonary artery and abolished RhoA-mediated calcium sensitisation of contraction, accounting for the decreased responses to endothelin-1, noradrenaline and a thromboxane analogue, and treatment with sildenafil at 25 milligrams per kilogram daily throughout the exposure prevented the downregulation of RhoA, the reduction of contraction and the pulmonary artery remodelling, indicating a major role of the nitric oxide and cyclic GMP pathway in the altered RhoA signalling.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sildenafil-research/12946946.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ce3f4a451c01082a280ebffc7e9661ec5667161f4974b39ba15c52fa940754f7", "start_char": 0, "end_char": 1768, "text_sha256": "ce3f4a451c01082a280ebffc7e9661ec5667161f4974b39ba15c52fa940754f7"}
- experimental_model
- Rat pulmonary artery contractility and RhoA expression after two weeks of chronic hypoxia
- exposure
- Sildenafil 25 milligrams per kilogram daily through two weeks of 10 percent oxygen, with real-time PCR and western blotting
- limitations
- Identifies a second arm of the mechanism beyond cyclic-GMP-mediated relaxation. A rat chronic hypoxia model, and the causal chain from cyclic GMP to RhoA expression is inferred rather than dissected.
- nutrient_topic
- Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. · Sildenafil
- organism
- Rat
- plain_language
- Beyond relaxing the vessel, the drug preserved the contractile machinery that chronic low oxygen otherwise degrades.
- primary_references
- [sil-p12946946] Sildenafil prevents change in RhoA expression induced by chronic hypoxia in rat pulmonary artery. (2003). https://pubmed.ncbi.nlm.nih.gov/12946946/ DOI: 10.1161/01.res.0000093220.90027.d9
- tissue_or_cell_type
- Pulmonary artery
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat pulmonary artery contractility and RhoA expression after two weeks of chronic hypoxia · source_derived_draft · unverified_draft
### sil-prevents-rhoa-downregulation Chronic hypoxia decreased RhoA messenger RNA and protein expression in rat main pulmonary artery and abolished RhoA-mediated calcium sensitisation of contraction, accounting for the decreased responses to endothelin-1, noradrenaline and a thromboxane analogue, and treatment with sildenafil at 25 milligrams per kilogram daily throughout the exposure prevented the downregulation of RhoA, the reduction of contraction and the pulmonary artery remodelling, indicating a major role of the nitric oxide and cyclic GMP pathway in the altered RhoA signalling. Condition category: normal nutrient_topic: Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. plain_language: Beyond relaxing the vessel, the drug preserved the contractile machinery that chronic low oxygen otherwise degrades. organism: Rat tissue_or_cell_type: Pulmonary artery experimental_model: Rat pulmonary artery contractility and RhoA expression after two weeks of chronic hypoxia limitations: Identifies a second arm of the mechanism beyond cyclic-GMP-mediated relaxation. A rat chronic hypoxia model, and the causal chain from cyclic GMP to RhoA expression is inferred rather than dissected. exposure: Sildenafil 25 milligrams per kilogram daily through two weeks of 10 percent oxygen, with real-time PCR and western blotting evidence_span: {"source_cache": "artifacts/sildenafil-research/12946946.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ce3f4a451c01082a280ebffc7e9661ec5667161f4974b39ba15c52fa940754f7", "start_char": 0, "end_char": 1768, "text_sha256": "ce3f4a451c01082a280ebffc7e9661ec5667161f4974b39ba15c52fa940754f7"} [sil-p12946946] Sildenafil prevents change in RhoA expression induced by chronic hypoxia in rat pulmonary artery. (2003). https://pubmed.ncbi.nlm.nih.gov/12946946/ DOI: 10.1161/01.res.0000093220.90027.d9
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.