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Articles in PresS, published online ahead of print April 4, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00675.2001
Submitted on November 12, 2001
Accepted on March 28, 2002
1 Department of Pediatrics, Research Institute Growth and Development (GROW), University Hospital Maastricht and Maastricht University, Maastricht, Limburg, The Netherlands
2 Department of Pharmacology & Toxicology, Cardiovascular Research Institute Maastricht(CARIM), University Hospital Maastricht and Maastricht University, Maastricht, Limburg, The Netherlands; School of Life Sciences, Transnational University Limburg, Maastricht, Limburg, The Netherlands
* To whom correspondence should be addressed. E-mail: J.DeMey{at}farmaco.unimaas.nl.
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 cyclo-oxygenase, nor by depolarization plus Ca2+-channel blockade. When arteries were simultaneously exposed to NE and acetylcholine (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 peripheral arteries, acute hypoxia blunts agonist-induced contraction of the smooth muscle and inhibits stimulated EDRF 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.
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