Nonsteroidal antiinflammatory drugs and renal function.
Vasodilatory renal prostaglandins, especially PGE2 and PGI2, maintain renal blood flow and glomerular filtration rate under certain circumstances, especially clinical and experimental conditions accompanied by renal vasoconstriction and increased plasma concentrations of catecholamines, angiotensin, and vasopressin. Inhibition of arachidonate cyclooxygenase by nonsteroidal antiinflammatory drugs reduces renal PGE2 and PGI2, exaggerates renal vasoconstriction, and thereby decreases renal blood flow and glomerular filtration rates. Reversible acute renal failure can accompany the clinical use of prostaglandin inhibitory drugs.
D000809:Angiotensins / Q000502:physiology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001095:Arachidonic Acids / Q000378:metabolism / Q000502:physiology; D016861:Cyclooxygenase Inhibitors; D015232:Dinoprostone; D011464:Epoprostenol / Q000502:physiology; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D007674:Kidney Diseases / Q000188:drug therapy / Q000503:physiopathology; D009638:Norepinephrine / Q000502:physiology; D011453:Prostaglandins / Q000096:biosynthesis / Q000502:physiology*; D011458:Prostaglandins E / Q000502:physiology; D012079:Renal Circulation / Q000187:drug effects; D013467:Sulindac / Q000494:pharmacology; D014661:Vasoconstriction; D014664:Vasodilation; D014667:Vasopressins / Q000502:physiology
D000809:Angiotensins; D000893:Anti-Inflammatory Agents; D001095:Arachidonic Acids; D016861:Cyclooxygenase Inhibitors; D011453:Prostaglandins; D011458:Prostaglandins E; D014667:Vasopressins; D013467:Sulindac; D011464:Epoprostenol; D015232:Dinoprostone; D009638:Norepinephrine