Korean J Physiol Pharmacol.  1998 Apr;2(2):209-216.

Hypoxia-induced EDNO release is further augmented by previous hypoxia and reoxygenation in rabbit aortic endothelium

Affiliations
  • 1Departments Thoracic Surgery, College of Medicine, Ewha Womans University, Seoul 158-056, Korea.
  • 2Departments of Physiology, College of Medicine, Ewha Womans University, Seoul 158-056, Korea.
  • 3Department of Thoracic Surgery, Seoul National University College of Medicine, Seoul, Korea.
  • 4Department of Physiology & Biophysics, Seoul National University College of Medicine, Seoul, Korea.

Abstract

The present study was designed: (1) to determine whether or not hypoxia stimulates the release of endothelium-derived relaxing factors (EDRFs) from endothelial cells, and (2) to examine whether or not the hypoxia-induced EDRFs release is further augmented by previous hypoxia-reoxygenation, using vessel and rabbit carotid artery without endothelium as a bioassay test ring. The test ring was contracted by prostaglandin F2alpha, (3 X 10-6 M/L), which was added to the solution perfuming through the aortic segment. Hypoxia was evoked by switching the solution aerated with 95% 02/5% CO2 mixed gas to one aerated with 95% N2/5% CO2 mixed gas. When the contraction induced by prostaglandin F2alpha reached a steady state, the solution was exchanged for hypoxic one. And then, hypoxia and reoxygenation were interchanged at intervals of 2 minutes (intermittent hypoxia). The endothelial cells were also exposed to single 10-minute hypoxia (continuous hypoxia). When the bioassay ring was superfused with the perfusate through intact aorta, hypoxia relaxed the precontracted bioassay test ring markedly. Whereas, when bioassay ring was superfused with the perfusate through denuded aorta or polyethylene tubing, hypoxia relaxed the precontracted ring slightly. The relaxation was not inhibited by indomethacin but by nitro-L-arginine or methylene blue. The hypoxia-induced relaxation was further augmented by previous hypoxia-reoxygenation and the magnitude of the relaxation by intermittent hypoxia was significantly greater than that of the relaxation by continuous hypoxia. The results suggest that hypoxia stimulates EDNO release from endothelial cells and that the hypoxia-induced EDNO release is further augmented by previous hypoxia-reoxygenation.

Keyword

Endothelium; Nitric oxide; Hypoxia; Reoxygenation

MeSH Terms

Anoxia*
Aorta
Biological Assay
Carotid Arteries
Dinoprost
Endothelial Cells
Endothelium*
Endothelium-Dependent Relaxing Factors
Indomethacin
Methylene Blue
Nitric Oxide
Polyethylene
Relaxation
Dinoprost
Endothelium-Dependent Relaxing Factors
Indomethacin
Methylene Blue
Nitric Oxide
Polyethylene
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