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
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- 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
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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.