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1 Department of Pediatrics, Research Institute Growth and Development and 2 Department of Pharmacology & Toxicology, Cardiovascular Research Institute Maastricht, University Hospital Maastricht and Maastricht University, 6200 MD Maastricht, The Netherlands
In the chicken embryo, acute hypoxemia
results in cardiovascular responses, including an increased peripheral
resistance. We investigated whether local direct effects of decreased
oxygen tension might participate in the arterial response to hypoxemia in the chicken embryo. Femoral arteries of chicken embryos were isolated at 0.9 of incubation time, and the effects of acute hypoxia on
contraction and relaxation were determined in vitro. While hypoxia
reduced contraction induced by high K+ to a small extent
(
21.8 ± 5.7%), contractile responses to exogenous norepinephrine (NE) were markedly reduced (51.1 ± 3.2%) in
80% of the arterial segments. This effect of hypoxia was not altered by removal of the endothelium, inhibition of NO synthase or
cyclooxygenase, or by depolarization plus Ca2+ channel
blockade. When arteries were simultaneously exposed to NE and ACh,
hypoxia resulted in contraction (+49.8 ± 9.3%). Also, relaxing
responses to ACh were abolished during acute hypoxia, while the vessels
became more sensitive to the relaxing effect of the NO donor sodium
nitroprusside (pD2: 5.81 ± 0.21 vs. 5.31 ± 0.27). Thus, in chicken embryo femoral arteries, acute hypoxia blunts
agonist-induced contraction of the smooth muscle and inhibits stimulated endothelium-derived relaxation factor release. The consequences of this for in vivo fetal hemodynamics during acute hypoxemia depend on the balance between vasomotor influences of circulating catecholamines and those of the endothelium.
catecholamine; endothelium-derived relaxation factor
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