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Am J Physiol Heart Circ Physiol (August 1, 2002). doi:10.1152/ajpheart.00151.2002
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Articles in PresS, published online ahead of print August 1, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00151.2002
Submitted on February 25, 2002
Accepted on July 24, 2002

Nucleoside Reverse Transcriptase Inhibitors Impair Endothelium-Dependent Relaxation by Increasing Superoxide

Roy L Sutliff1*, Sergey Dikalov2, Daiana Weiss2, Jeremy D Parker1, Scott M Raidel1, Andrea K Racine1, Rodney B Russ1, Chad P Haase1, W. Robert Taylor2, and William Lewis1

1 Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA, USA
2 Department of Medicine, Division of Cardiology, Emory University, Atlanta, GA, USA

* To whom correspondence should be addressed. E-mail: rsutlif{at}emory.edu.

Nucleoside reverse transcriptase inhibitors (NRTI) have been used successfully to reduce AIDS mortality. However, the use of these compounds is associated with numerous tissue toxicities including cardiomyopathy. Studies herein address the effects of NRTIs on vascular function. Functional assays of contraction and relaxation were performed on isolated mouse aorta segments obtained from FVB/n mice exposed to zidovudine (AZT), stavudine (D4T), or water for 35 days. Both AZT and D4T treatment impaired sensitivity to endothelium-dependent relaxation by acetylcholine. Dihydroethidium staining revealed that AZT treatment was associated with an increase in superoxide levels. Pretreatment of AZT-treated vessels with tiron (1 mM), a free radical scavenger, restored endothelium-dependent relaxation in AZT-treated mice. In cellular preparations, ESR measurements revealed elevated superoxide in cultured endothelial cells exposed to AZT; elevation was dependent on the length of exposure. These results indicate that NRTIs impair endothelium-dependent relaxation by increasing superoxide levels and suggest that NRTI therapy contributes to cardiovascular complications in AIDS.




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