TP and/or EP3 receptors mediate the vasoconstrictor and pressor responses of prostaglandin F2α in mice and/or humans

What is it about?

Cyclooxygenase (COX) is an enzyme in mammal to participate in converting arachidonic acid into 1 or several of 5 prostanoids, namely prostaglandin I2 (PGI2), PGE2, PGD2, PGF2a, and thromboxane A2, depending on the downstream corresponding synthase(s) in a specific tissue. COX pathways are involved in various physiological and pathophysiological processes and are therapeutic targets of many diseases. COX-derived prostanoids have long been considered to exert their biologic effects via acting on their respective receptors. Among them, PGF2alpha is clinically used as a therapeutic for uterine atony, a major cause of postpartum hemorrhage that leads to maternal morbidity. However, the vasoconstrictor and/or pressor effects of PGF2a limits the clinical use of the agent and implicates in the development of vascular pathologies such as hypertension and atherosclerosis. In the present study by using mice deficient of thromboxane-prostanoid receptor (TP) and/or E prostanoid receptor-3 (EP3) , and vessels from humans, we demonstrated that TP and/or EP3 rather than the prototype receptor of the prostanoid, i.e., FP that mediates uterine contraction are responsible for the vasoconstrictor and pressor effects of PGF2a, which are still of concern under clinical conditions.

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