Platelet aggregation is caused by ?
Ans. is 'b' i.e., Thromboxane A2 Platete aggregation Platelate mechanism cAMP plays a key role in platelet mechanism- antiaggregatory or aggregatory. High concentration of cAMP inhibit platelet adhesion, aggregation and the release of active substances. Low concentration of cAMP has an opposite effect. cAMP is formed by the action of enzyme adenylate cyclase and degraded by phosphodiesterase. Thromboxane A2 (synthesized in platelets) and ADP inhibit adenylate cyclase - cAMP --) Platelet aggregation and adhesion. Prostacyclin PGI2 (Synthesized in endothelium) stimulates adenylate cyclase cAMP -* antiaggregatory effect Prostacyclin and thromboxane A, are synthesized from prostaglandins that are formed from arachidonic acid by the action of cycloxygenase. Platelet activation Circulating resting platelets do not stick to healthy endothelium or each other. When there is damage to endothelium, constituents of the subendothelial matrix are exposed especially collagen and von willebrand factor. Platelets attach to these matrix constituents and there is simultaneous release of thromboxane - A2 (TXA 2)and adenosine diphosphate. TX.4 2 and ADP are proaggregatory and vasoconstrictor mediators - they promote recruitment of additional platelets. These platelets bind to adhesive proteins like fibrinogen or fibrin and von willebrand factor through surface integrin glycoprotein GP Ila/Illb formation of platelet plug. Injury to the blood vessel 1. Transient vasoconstriction and Platelet adhesion to VWF because of Gp Ib receptor Platelets release aggregating agents like ADP and conformational change in Gp IIb-IIIa receptor Synthesis of thromboxane A2 by platelets (Tx A2 causes vasoconstriction and increase attachment of fibrinogen to the Gp IIb-illa receptor Platelets held together by fibrinogen resulting information of temporary platelet plug Thrombin conves fibrinogen into fibrin and formation of stable platelet plug (platelet hod together by fibrin)
Nitrous oxide
Thromboxone A2
Aspirin
PGI2