The Role of Arachidonic Acid Metabolism in the Modulation of Renal Blood Flow
Cellular elements located in the collecting tubules,1 the glomeruli,2 the medullary interstitium,3 and the blood vessels of the kidney4 have the capacity to metabolize arachidonic acid to an endoperoxide intermediate that is the immediate precursor of thromboxane A2 and prostaglandins (PG) E2, F2α, D2, and I2. In 1970 McGiff et al. reported that release of renal prostaglandins during close arterial infusion of angiotensin II in the dog was associated with waning of the renal vasoconstrictor action of the peptide, and suggested involvement of renal prostaglandins in the regulation of blood flow to the kidney.5 This concept gained strength over the past decade with the demonstration that vasoactive hormones including angiotensin and norepinephrine stimulate renal prostaglandin synthesis, that several prostaglandins reduce the tone and reactivity of the renal vasculature to vasoconstrictor hormones, that induction of renal prostaglandin synthesis during infusion of arachidonic acid is associated with vasodilation and increased blood flow to the kidney, and that inhibitors of prostaglandin synthesis bring about renal vasoconstriction and lowering of the blood flow in a number of states characterized by enhanced activity of one or more vasoconstrictor neurohormonal systems. Hence it is now apparent that an interplay between renal prostaglandins and the renin—angiotensin and/or sympathetic nervous system is a dominant feature of mechanisms regulating the blood flow to the kidney. This review analyzes the relationships between renal prostaglandins and vasoconstrictor systems and discusses the significance of such relationships with regard to the renal circulation.
KeywordsArachidonic Acid Plasma Renin Activity Renal Blood Flow Mean Arterial Blood Pressure Prostaglandin Synthesis
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