mentioned deleterious cardiovascular profile of NSAIDs can be accounted for by inhibition of .Following the COX-mediated synthesis of PGH 2 from arachidonate, PGH 2 is metabolized to one of at least five bioactive prostaglandins, including PGE 2 , PGI 2 , PGF 2 , PGD 2 , or thromboxane A 2 (TxA 2 ) (5,11,12).These prostanoids have pleiotropic cardiovascular effects altering platelet function (13-15) and renal function (2), and acting either as vasodilators or vasoconstrictors (16)(17)(18)(19).Whereas PGI 2 is a vasodilator (18, 20), TxA 2 is a vasoconstrictor (8, 21), while PGE 2 , which may interact with four distinct receptors, can act either as a vasodilator or a vasoconstrictor depending on the accessibility of the specific receptors (16,22).Although COX1 and COX2 exhibit similar biochemical activity in converting arachidonate to PGH 2 in vitro (13, 23), the ultimate prostanoids they produce in vivo may be different (15, 24) due to differential regulation of COX1 and COX2 (6,7,25,26), tissue distribution (2,25,26), and availability of the downstream prostanoid synthases (24,27,28).Given the potential heterogeneity in the spectrum of prostanoids synthesized by a given cell, and the available downstream receptors, the net effect of COX inhibition on the cardiovascular system may be quite unpredictable.
No takes yet. Share an insight, caveat, or question.
Qi et al. (2002) studied this question.