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Articles in PresS, published online ahead of print February 25, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00347.2001
Submitted on November 27, 2001
Accepted on February 8, 2002
1 Institut fur Pharmakologie, Universitat Regensburg, Regensburg, Germany
2 Innere Medizin II, Universitatsklinikum Regensburg, Regensburg, Germany
3 Institut fur Anatomie, Universitat Regensburg, Regensburg, Germany
4 Institut fur Physiologie, Universitat Regensburg, Regensburg, Germany
* To whom correspondence should be addressed. E-mail: klaus.hoecherl{at}chemie.uni-regensburg.de.
We investigated the impact of cyclooxygenase (COX) activity for the regulation of the renin-angiotensin-aldosterone system by salt intake. Therefore, Sprague-Dawley rats were subjected to different salt diets (0.02%, 0.6% and 8% NaCl, wt/wt) and treated with the selective COX-2 inhibitor rofecoxib (10 mg/kg x d) or with ketorolac at a dose selective for COX-1 inhibition (2 mg/kg x d) for 3, 7, 14 and 21 days. Rofecoxib and Ketorolac caused a similar reduction of renocortical prostaglandin E2 (PGE2) formation with low salt diet. Rofecoxib did not change plasma renin activity (PRA) nor renocortical renin mRNA abundance at any salt diet, but clearly lowered plasma aldosterone concentration (PAC). In contrast, Ketorolac delayed the increase of PRA and of renin mRNA in response to low salt intake but did not change PAC. Prolonged treatment with rofecoxib but not with ketorolac caused an upregulation of COX-2 expression whilst COX-1 mRNA abundance remained unchanged. These findings suggest that COX-1 but not COX-2 derived prostanoids are of relevance for the regulation of the renin system by salt intake.
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