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Am J Physiol Regul Integr Comp Physiol 270: R1126-R1131, 1996;
0363-6119/96 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 270, Issue 5 1126-R1131, Copyright © 1996 by American Physiological Society

ARTICLES

Hypoxia-reoxygenation impairs endothelium-dependent relaxation in isolated rat aorta

S. Yokoyama, R. J. Korthuis and J. N. Benoit
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130, USA.

The effects of hypoxia followed by reoxygenation on endothelium-dependent relaxation in isolated rat aorta were investigated. Acetylcholine (ACh, 3 nM-10 microM) and calcium ionophore A-23187 (3 nM-300 nM)-induced endothelium-dependent vasorelaxation of isolated rate aortic vessel rings was impaired after 15 min of hypoxia followed by 30 min of reoxygenation. Impairment of ACh-induced relaxation was prevented by pretreatment with the combination of superoxide dismutase (200 U/ml) and catalase (1,000 U/ml). Hypoxia-reoxygenation did not affect sodium nitroprusside (0.1 nM-1 microM)-induced endothelium-independent relaxation nor the dissociation constant of ACh to endothelial M3 muscarinic receptors. Propidium iodide staining of the vascular endothelium revealed a significant increase in the number of dead endothelial cells on the aortic vessel rings following hypoxia-reoxygenation, but not on those pretreated with superoxide dismutase and catalase. These results suggest that hypoxia-reoxygenation impairs endothelium-dependent relaxation of rat aorta by a mechanism that involves oxidant-mediated endothelial cell death.


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