From the Guidelines
The inhibitor of platelet aggregation is prostacyclin I. Prostacyclin is produced by endothelial cells lining blood vessels and acts as a natural antiplatelet agent, as stated in 1 and further supported by 1. It works by increasing cyclic AMP levels in platelets, which inhibits platelet activation and aggregation. This contrasts with thromboxane A2, which promotes platelet aggregation. Adenosine diphosphate, serotonin, and von Willebrand's factor all promote platelet aggregation rather than inhibit it.
Key Points
- Prostacyclin causes vasodilation, further helping to prevent thrombus formation by improving blood flow.
- The balance between prostacyclin and pro-aggregatory factors is crucial for normal hemostasis, and disruption of this balance can lead to either bleeding disorders or thrombotic conditions, as discussed in 1.
- Prostacyclin has antiproliferative properties and is a potent vasodilator, whereas thromboxane A2 is a potent vasoconstrictor and promotes proliferation and platelet activation, as mentioned in 1.
Mechanism of Action
Prostacyclin's mechanism of action involves increasing cyclic AMP levels in platelets, leading to inhibition of platelet activation and aggregation. This is in line with the findings reported in 1, which highlights the importance of prostacyclin in vascular health.
Clinical Implications
Understanding the role of prostacyclin in inhibiting platelet aggregation is crucial for managing conditions related to thrombosis and hemostasis, and therapies targeting the prostacyclin pathway may offer benefits in these contexts, as implied by the discussions in 1 and 1.
From the FDA Drug Label
Epoprostenol (PGI2, PGX, prostacyclin), a metabolite of arachidonic acid, is a naturally occurring prostaglandin with potent vasodilatory activity and inhibitory activity of platelet aggregation. Epoprostenol has 2 major pharmacological actions: (1) direct vasodilation of pulmonary and systemic arterial vascular beds, and (2) inhibition of platelet aggregation.
The inhibitor of platelet aggregation is:
- prostacyclin (also known as epoprostenol) 2, 2, 2 The other options (thromboxane A2, adenosine diphosphate, serotonin, von Willebrand’s factor) are not supported by the provided drug labels as inhibitors of platelet aggregation in the context of the question.
From the Research
Inhibitor of Platelet Aggregation
The correct answer is: prostacyclin I
- Prostacyclin is a potent inhibitor of platelet aggregation, as stated in the studies 3, 4, 5
- It is the most potent endogenous inhibitor of platelet aggregation yet discovered, both inhibiting aggregation and dispersing existing aggregates 3
- Prostacyclin inhibits aggregation through stimulation of platelet adenyl cyclase leading to an increase in platelet cyclic AMP 4
- The other options are not correct because:
- Thromboxane A2 is a potent vasoconstrictor and stimulus of platelet aggregation, not an inhibitor 6
- Adenosine diphosphate (ADP) is an aggregating agent that induces platelet aggregation, not an inhibitor 7
- Serotonin is not mentioned as an inhibitor of platelet aggregation in the provided studies
- Von Willebrand’s factor is not mentioned as an inhibitor of platelet aggregation in the provided studies