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Endothelial dysfunction is induced by proinflammatory oxidant hypochlorous acid
C Zhang1, R Patel, J P Eiserich
1Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
American Journal of Physiology. Heart and Circulatory Physiology
|September 15, 2001
Summary
Hypochlorous acid (HOCl), an inflammatory oxidant, impairs blood vessel function by reducing nitric oxide (NO) availability. This endothelial dysfunction is linked to alterations in L-arginine metabolism.
Area of Science:
- Biochemistry
- Physiology
- Vascular Biology
Background:
- Myeloperoxidase (MPO)-derived hypochlorous acid (HOCl) is implicated in inflammatory tissue injury.
- Nitric oxide (NO) is a critical regulator of vascular function and tone.
Purpose of the Study:
- To investigate the effect of HOCl on nitric oxide (NO) bioavailability in rat aortic rings.
- To determine the mechanism by which HOCl affects endothelial function.
Main Methods:
- Rat aortic ring segments were treated with varying concentrations of HOCl.
- Endothelium-dependent relaxation was assessed using acetylcholine (ACh) and calcium ionophore A23187.
- Endothelium-independent relaxation was measured with sodium nitroprusside.
- Endothelial NO synthase (eNOS) activity and NO metabolite formation were analyzed in bovine aortic endothelial cells.
- The role of L-arginine was investigated by assessing the reversal of HOCl's effects.
Main Results:
- HOCl significantly impaired endothelium-dependent relaxation induced by ACh and A23187.
- HOCl did not affect endothelium-independent relaxation to sodium nitroprusside.
- The inhibitory effect of HOCl was reversed by L-arginine, but not D-arginine.
- HOCl reduced NO metabolite (nitrate and nitrite) formation in endothelial cells.
- HOCl did not alter eNOS protein or activity.
Conclusions:
- HOCl induces endothelial dysfunction by interfering with L-arginine, leading to decreased NO bioavailability.
- This mechanism contributes to vascular injury during inflammation.