Journal
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
Volume 17, Issue 1, Pages 64-69Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MNH.0b013e3282f1bb7d
Keywords
angiotensin; cyclooxygenase-2; hypertension; prostaglandin; renin
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Funding
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK062794] Funding Source: NIH RePORTER
- NIDDK NIH HHS [DK-62794, DK3961] Funding Source: Medline
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Purpose of review This review highlights recent studies examining the expression and function of cyclooxygenase-2 and its metabolites in the kidney. Recent findings Expression of cyclooxygenase-2 is regulated by both physiologic and pathophysiologic perturbations, with volume depletion upregulating macula-densa expression and volume expansion upregulating medullary expression. Macula densa cyclooxygenase-2 is a modulator of juxtaglomerular renin expression, and there is increasing evidence that cyclooxygenase-2 expression is modulated by multiple components of the renin-angiotensin system, including angiotensin II, through both AT1 and AT2 receptors. There are also indications that macula densa cyclooxygenase-2 expression may be regulated by the prorenin/renin receptor. Medullary cyclooxygenase-2 metabolites modulate salt and water excretion, and cyclooxygenase-2 inhibitors lead to sodium and volume retention and may raise blood pressure. There is also increasing evidence that cyclooxygenase-2 expression increases in progressive renal injury. Given their cardiovascular and renal side effects, cyclooxygenase-2 inhibitors are not a feasible intervention for long-term therapy against progressive renal damage, but further delineation of the downstream receptors and synthases involved may provide therapeutic targets. Summary Recent studies have highlighted the important role that cyclooxygenase-2 metabolites play both in regulation of normal renal function and as potential mediators of acute and chronic renal injury.
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