Prostacyclin synthesis by the vessel wall: molecular mechanisms & dependencies

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.

Human evidence only

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

Two hours after 150 or 300 milligrams of aspirin, 81 to 100% inhibition of vein-wall prostacyclin synthesis was demonstrated with 86% inhibition still evident in one subject at eight hours, while platelet thromboxane B2 production was completely inhibited for more than 24 hours, leading to the conclusion that there is little difference between the initial inhibitory response of platelet cyclooxygenase and that of vessel-wall cyclooxygenase to these doses, and that the prolonged bleeding time after aspirin is not a consequence of selective inhibition of platelet thromboxane production.
Aspirin / acetylsalicylic acid → Prostacyclin synthesis by the vessel wall source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Vein segments and platelets sampled from five subjects before and after aspirin, with radioimmunoassay of stable metabolites
exposure
150 or 300 milligrams of oral aspirin
limitations
Five subjects, and the vein segments are surgically obtained rather than sampled in situ. Its conclusion is the opposite of the low-dose study in this collection and the doses differ tenfold.
nutrient_topic
Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
organism
Human
plain_language
At ordinary tablet doses the vessel wall is hit about as hard as the platelet.
primary_references
[asa-p7003384] Inhibition of prostacyclin and platelet thromboxane A2 after low-dose aspirin. (1981). https://pubmed.ncbi.nlm.nih.gov/7003384/ DOI: 10.1056/nejm198101083040203
tissue_or_cell_type
Vein wall and platelets
Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 377–388
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Vein segments and platelets sampled from five subjects before and after aspirin, with radioimmunoassay of stable metabolites · source_derived_draft · unverified_draft
### asa-no-selectivity-at-higher-dose Two hours after 150 or 300 milligrams of aspirin, 81 to 100% inhibition of vein-wall prostacyclin synthesis was demonstrated with 86% inhibition still evident in one subject at eight hours, while platelet thromboxane B2 production was completely inhibited for more than 24 hours, leading to the conclusion that there is little difference between the initial inhibitory response of platelet cyclooxygenase and that of vessel-wall cyclooxygenase to these doses, and that the prolonged bleeding time after aspirin is not a consequence of selective inhibition of platelet thromboxane production. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: At ordinary tablet doses the vessel wall is hit about as hard as the platelet. organism: Human tissue_or_cell_type: Vein wall and platelets experimental_model: Vein segments and platelets sampled from five subjects before and after aspirin, with radioimmunoassay of stable metabolites limitations: Five subjects, and the vein segments are surgically obtained rather than sampled in situ. Its conclusion is the opposite of the low-dose study in this collection and the doses differ tenfold. exposure: 150 or 300 milligrams of oral aspirin evidence_span: {"source_cache": "artifacts/aspirin-research/7003384.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b54b61e084b6ec232b9c86ef5de713b0d5a57def2525eb6d3d50e5d7768e5c38", "start_char": 0, "end_char": 1148, "text_sha256": "b54b61e084b6ec232b9c86ef5de713b0d5a57def2525eb6d3d50e5d7768e5c38"} [asa-p7003384] Inhibition of prostacyclin and platelet thromboxane A2 after low-dose aspirin. (1981). https://pubmed.ncbi.nlm.nih.gov/7003384/ DOI: 10.1056/nejm198101083040203
Complete structured claim and evidence

Where it participates (unsigned role)

In rabbits lower doses of aspirin produced major inhibition of platelet aggregation and minor inhibition of prostacyclin synthesis while higher doses inhibited both, in humans a dose equivalent to approximately one quarter of one 300 milligram tablet consistently produced major inhibition of cyclooxygenase-dependent platelet aggregation in a pattern similar to that in rabbits where most prostacyclin synthetic capacity was not inhibited, and it took rabbit vasculature over 24 hours to return to control prostacyclin synthetic capacity after a single high dose.
Aspirin / acetylsalicylic acid → Cyclooxygenase-dependent platelet aggregation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/aspirin-research/6156337.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0d904fae5d8c006bd180213b6b2cbc88c87bb103b9c8b8872705330c349b074", "start_char": 0, "end_char": 1502, "text_sha256": "e0d904fae5d8c006bd180213b6b2cbc88c87bb103b9c8b8872705330c349b074"}
experimental_model
Human and rabbit platelet aggregation with rabbit aortic prostacyclin synthesis measured across aspirin doses
exposure
Graded oral aspirin doses, sampled three hours after dosing, with recovery followed over 24 hours in rabbits
limitations
Sets the dose at which the two tissues start to separate, but the vascular arm is rabbit aorta and the human arm measures aggregation rather than prostacyclin.
nutrient_topic
Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
organism
Human and rabbit
plain_language
About a quarter of a tablet stops the platelets while mostly leaving the vessel wall alone.
primary_references
[asa-p6156337] Effect of oral aspirin dose on platelet aggregation and vascular prostacyclin (PGI2) synthesis in humans and rabbits. (1980). https://pubmed.ncbi.nlm.nih.gov/6156337/ DOI: 10.1097/00005344-198007000-00006
tissue_or_cell_type
Platelets and aorta
Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 390–401
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and rabbit platelet aggregation with rabbit aortic prostacyclin synthesis measured across aspirin doses · source_derived_draft · unverified_draft
### asa-a-quarter-tablet In rabbits lower doses of aspirin produced major inhibition of platelet aggregation and minor inhibition of prostacyclin synthesis while higher doses inhibited both, in humans a dose equivalent to approximately one quarter of one 300 milligram tablet consistently produced major inhibition of cyclooxygenase-dependent platelet aggregation in a pattern similar to that in rabbits where most prostacyclin synthetic capacity was not inhibited, and it took rabbit vasculature over 24 hours to return to control prostacyclin synthetic capacity after a single high dose. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: About a quarter of a tablet stops the platelets while mostly leaving the vessel wall alone. organism: Human and rabbit tissue_or_cell_type: Platelets and aorta experimental_model: Human and rabbit platelet aggregation with rabbit aortic prostacyclin synthesis measured across aspirin doses limitations: Sets the dose at which the two tissues start to separate, but the vascular arm is rabbit aorta and the human arm measures aggregation rather than prostacyclin. exposure: Graded oral aspirin doses, sampled three hours after dosing, with recovery followed over 24 hours in rabbits evidence_span: {"source_cache": "artifacts/aspirin-research/6156337.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0d904fae5d8c006bd180213b6b2cbc88c87bb103b9c8b8872705330c349b074", "start_char": 0, "end_char": 1502, "text_sha256": "e0d904fae5d8c006bd180213b6b2cbc88c87bb103b9c8b8872705330c349b074"} [asa-p6156337] Effect of oral aspirin dose on platelet aggregation and vascular prostacyclin (PGI2) synthesis in humans and rabbits. (1980). https://pubmed.ncbi.nlm.nih.gov/6156337/ DOI: 10.1097/00005344-198007000-00006
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

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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.

Prostacyclin synthesis by the vessel wall