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Articles in PresS, published online ahead of print November 12, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00136.2002
Submitted on April 11, 2002
Accepted on November 11, 2002
1 Department of Medicine IV, University of Erlangen-Nurnberg, Erlangen, Germany
* To whom correspondence should be addressed. E-mail: karl.hilgers{at}rzmail.uni-erlangen.de.
Upregulation of the inducible cyclooxygenase (COX-2) in the macula densa accompanies the activation of the juxtaglomerular apparatus in many high-renin conditions. The functional role of COX-2 in these disease states is poorly understood. We tested whether COX-2 is required to increase renin in renovascular hypertension. Rats with established 2-kidney, 1-clip (2K1C) hypertension were treated for two weeks with two different inhibitors of COX-2, NS-398 and rofecoxib, respectively. Hypertension in 2K1C was not affected or slightly enhanced by COX-2 inhibition, as measured intraarterially in conscious animals. The increase of plasma renin activity was also unchanged by both rofecoxib and NS-398. The number of glomeruli with a renin-positive juxtaglomerular apparatus was elevated in clipped kidneys and decreased in contralateral kidneys of 2K1C. This pattern was unaltered by COX-2 inhibition. To test the effects of COX-2 blockade on an primarily macula densa-mediated stimulus, we studied salt depletion for comparison. Low-salt diet induced a significant increase of plasma renin activity, which was partially inhibited by treatment with NS-398. We conclude that inhibition of COX-2 in established renovascular hypertension does not affect renin synthesis or release. Thus, either COX-2 is not necessary for the macula densa mechanism, or the macula densa is not important for maintaining high renin in renovascular hypertension.
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