The Effect of Hypoxia on the Release of Endothelium-derived Relaxing Factor in Rabbit Thoracic Aorta.
- Author:
Soo Seung CHOI
1
Author Information
1. Department of Thoracic and Cardiovascular Surgery, Ewha Womans University School of Medicine, Korea. gratia@unitel.co.kr
- Publication Type:Original Article
- Keywords:
Endothelium;
Hypoxia;
Nitrous Oxide;
Calcium
- MeSH:
Anoxia;
Aorta;
Aorta, Thoracic;
Biological Assay;
Blood Vessels;
Carotid Arteries;
Deoxyglucose;
Endothelial Cells;
Endothelium;
Endothelium-Dependent Relaxing Factors;
Gases;
Isometric Contraction;
NG-Nitroarginine Methyl Ester;
Nitrous Oxide;
Relaxation;
Tea;
Tetraethylammonium
- From:The Korean Journal of Thoracic and Cardiovascular Surgery
2009;42(5):588-596
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: To clarify the effect of hypoxia on vascular contractility, we tried to show whether hypoxia induced the release of endothelium-derived relaxing factor (EDRF) and the nature of the underlying mechanism for this release. MATERIAL AND METHOD: Isometric contractions were observed in rabbit aorta, and the released EDRF from the rabbit aorta was bioassayed by using rabbit denuded carotid artery. The intracellular Ca2+ concentration ([Ca2+]i) in the cultured rabbit aortic endothelial cells was recorded by a microfluorimeter with using Fura-2/AM. Hypoxia was evoked to the blood vessels or endothelial cells by eliminating the O2 in the aerating gases in the external solution. Chemical hypoxia was evoked by applying deoxyglucose or CN-. RESULT: Hypoxia relaxed the precontracted rabbit thoracic aorta that had its endothelium, and the magnitude of the relaxation was gradually increased by repetitive bouts of hypoxia. In contrast, hypoxia-induced relaxation was not evoked in the aorta that was denuded of endothelium. In a bioassay experiment, hypoxia released endothelium-derived relaxing factor (EDRF) and the release was inhibited by L-NAME or the K+ channel blocker tetraethylammonium (TEA). In the cultured endothelial cells, hypoxia augmented the ATP-induced increase of the intracellular Ca2+ concentration ([Ca2+]i) and this increase was inhibited by TEA. Furthermore, chemical hypoxia also increased the Ca2+ influx. CONCLUSION: From these results, it can be concluded that hypoxia might induce the release of NO from rabbit aortic endothelial cells by increasing [Ca2+]i.
