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Article
June 15, 1984

Biosynthesis of Thromboxane A2 in Renovascular Hypertension

JAMA. 1984;251(23):3121-3122. doi:10.1001/jama.1984.03340470047025
Abstract

A variety of biologically active mediators are formed from arachidonic acid within the kidney. The most abundant metabolites are prostaglandins and thromboxane A2, formed via cyclic endoperoxide intermediates by the enzyme cyclooxygenase. These products are formed in response to phasic stimuli. They are not stored following synthesis, and their evanescent nature suggests that they are most likely to act locally as regulators of cellular homeostasis. Degradation products and metabolites of prostaglandins are generally biologically inactive. An exception is 6-keto-PGE1, a long-lived metabolite of prostacyclin formed by the enzyme 9α-hydroxy-prostaglandin-dehydrogenase. 6-Keto-PGE1, like prostacyclin, inhibits platelet aggregation, relaxes vascular smooth muscle, and is a potent renin secretagogue. However, although the kidney possesses the enzymatic machinery to generate 6-keto-PGE1, structural evidence that it is actually formed in vivo is still outstanding.

In several species, the predominant cyclooxygenase product formed within the renal cortex is prostacyclin, virtually the exclusive metabolite

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