Role of thromboxane A2 signaling in endothelium-dependent contractions of arteries

Thromboxane A(2) (TxA(2)) 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 TxA(2) signaling in endothelium-dependent contractions of arteries. Arachidonic acid (AA) is metabolized by cyclooxygenase (COX) to form the unstable prostaglandin H-2 which is further converted into TxA(2). After being produced by thromboxane synthase (TxAS), TxA(2) ultimately stimulates TxA(2)/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 TxA(2). 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 TxA(2) 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.