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Am J Physiol Heart Circ Physiol 283: H2363-H2370, 2002. First published August 1, 2002; doi:10.1152/ajpheart.00151.2002
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Vol. 283, Issue 6, H2363-H2370, December 2002

Nucleoside reverse transcriptase inhibitors impair endothelium-dependent relaxation by increasing superoxide

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

1 Department of Pathology and Laboratory Medicine and 2 Division of Cardiology, Department of Medicine, Emory University, Atlanta, Georgia 30322

Nucleoside reverse transcriptase inhibitors (NRTIs) have been used successfully to reduce acquired immunodeficiency syndrome mortality. However, the use of these compounds is associated with numerous tissue toxicities, including cardiomyopathy. These studies 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, or water for 35 days. AZT and stavudine 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 mice. In cellular preparations, electron spin resonance 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 acquired immunodeficiency syndrome.

vascular; reactive oxygen species; nitric oxide; zidovudine; stavudine


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