Cyclooxygenase-2 in the Kidney

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Abstract
Prostaglandins play myriad roles as local mediators of inflammation and as modulators of physiologic functions, such as maintenance of gastric mucosal integrity and modulation of renal microvascular hemodynamics, renin release, and tubular salt and water reabsorption (2). After the recognition that COX was the target of aspirin (3), the pharmaceutical industry developed a substantial number of nonsteroidal anti-inflammatory drugs (NSAID), whose mechanism of action involves competitive or noncompetitive inhibition of COX activity. However, by the early 1990s, experimental studies began to suggest that COX-1 might not be the enzyme responsible for increased prostanoid production in inflammatory states. In cultured cells and tissue, COX activity increased rapidly in response to mitogens and cytokines (4,5,6), although COX-1 mRNA and immunoreactive protein were not altered. Furthermore, glucocorticoid administration was shown to decrease COX activity in peritoneal macrophages after lipopolysaccharides (7) but not to affect constitutive renal medullary COX activity. These results led Needleman and co-workers (7) to postulate the existence of a second, inflammatory-mediated COX isoform.

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