Abstract
The issues raised by Tsikas and Stichtenoth1 in their letter with regard to our article2 fall into 2 areas: (1) the possible endothelial NOS (eNOS)–cyclooxygenase (COX)-2 interaction and products of COX-2 activation; (2) the cardiovascular protection by coxibs. Concerning the first issue, we agree that a cross-talk between eNOS and COX-2 exists. Vascular eNOS expression was not investigated because it was beyond the scope of our study. Nevertheless, our functional experiments indirectly indicate that the decreased eNOS activity secondary oxidative stress generation, if occurring, is a surmountable and temporary phenomenon. Indeed, the sensitivity to L-NAME was acutely restored when vascular oxidative stress was inhibited by the scavenger ascorbic acid or COX-2 blockade, suggesting that NO production is quickly restored after …
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