Thromboxane A2 (TXA2) and prostacyclin (PGI2) are both derived from arachidonic acid via the cyclooxygenase pathway. They have opposing effects on platelet aggregation and vascular tone. The enzyme that synthesises TXA2 in platelets and the receptor through which it promotes aggregation are:

• A Prostacyclin synthase; IP receptor (Gs-coupled, increases cAMP)
• B Thromboxane synthase; IP receptor (Gi-coupled, decreases cAMP)
• C Thromboxane synthase; TP receptor (Gq-coupled, increases intracellular Ca2+) ✓
• D PGI2 synthase; TP receptor (Gs-coupled, activates adenylate cyclase)

Explanation

Thromboxane synthase in platelets converts PGH2 to TXA2, which acts on the TP receptor (thromboxane-prostanoid receptor), a Gq-protein coupled receptor. Gq activation increases intracellular Ca2+ via IP3 generation from PLC, promoting platelet activation and vasoconstriction. PGI2 (prostacyclin), synthesised by prostacyclin synthase in endothelial cells, acts on the IP receptor (Gs-coupled), raising cAMP via adenylate cyclase, which inhibits platelet aggregation and causes vasodilation. The opposing TXA2/PGI2 balance is the biochemical basis for low-dose aspirin's antithrombotic effect: aspirin irreversibly acetylates COX, but anucleate platelets cannot regenerate COX, while endothelial cells can.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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