Thromboxane A2 (TxA2) plays a very important role in various cardiovascular diseases through its action on platelet aggregation, vasoconstriction, and proliferation. The present article focuses on the role of TxA2 signaling in endothelium-dependent contractions of arteries. Arachidonic acid (AA) is metabolized by cyclooxygenase (COX) to form the unstable prostaglandin H2 which is further converted into TxA2. After being produced by thromboxane synthase (TxAS), TxA2 ultimately stimulates TxA2/prostanoid (TP) receptor to induce vasoconstriction. The calcium ionophore A23187, the prostanoid precursor AA, or the muscarinic receptor agonist acetylcholine (ACh) can evoke endothelium-dependent contractions associated with TxA2. The endothelium-dependent contractions shown in hypertension, diabetes, atherogenesis, and other cardiovascular diseases have been significantly reduced by antagonism of COX, TxAS, or TP receptor. So inhibition of the bioavailability and/or effect of TxA2 may be promising therapeutic targets to prevent these diseases. Especially some bioactive compounds isolated from medicinal plants will provide new pharmacological approaches to promote vascular health.
Keywords: Arteries; Endothelium-dependent contractions; Thromboxane A(2).
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