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1 Departments of Medicine, Vascular Biology and Hypertension Program, 2 Pathology, 3 Anesthesiology, and 4 Center for Free Radical Biology, University of Alabama at Birmingham; Birmingham, Alabama 35294; and 5 Division of Nephrology, Department of Internal Medicine, University of California at Davis, Davis, California 95616
The myeloperoxidase (MPO)-derived oxidant
hypochlorous acid (HOCl) plays a role in tissue injury under
inflammatory conditions. The present study tests the hypothesis that
HOCl decreases nitric oxide (NO) bioavailability in the vasculature of
Sprague-Dawley rats. Aortic ring segments were pretreated with HOCl
(1-50 µM) followed by extensive washing. Endothelium-dependent
relaxation was then assessed by cumulative addition of acetylcholine
(ACh) or the calcium ionophore A23187. HOCl treatment significantly impaired both ACh- and A23187-mediated relaxation. In contrast, endothelium-independent relaxation induced by sodium nitroprusside was
unaffected. The inhibitory effect of HOCl on ACh-induced relaxation was
reversed by exposure of ring segments to L-arginine but not D-arginine. In cellular studies, HOCl did not alter
endothelial NO synthase (NOS III) protein or activity, but inhibited
formation of the NO metabolites nitrate (NO
nitric oxide; endothelium; smooth muscle
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