Direct effects of acute hypoxia on the reactivity of peripheral arteries of the chicken embryo

Abstract

. Direct effects of acute hypoxia on the reactivity of peripheral arteries of the chicken embryo. Am J Physiol Regulatory Integrative Comp Physiol 283: R331-R338, 2002. First published April 4, 2002 10.1152/ajpregu.00675.2001.-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 ϩ to a small extent (Ϫ21.8 Ϯ 5.7%), contractile responses to exogenous norepinephrine (NE) were markedly reduced (Ϫ51.1 Ϯ 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 Ca 2ϩ channel blockade. When arteries were simultaneously exposed to NE and ACh, hypoxia resulted in contraction (ϩ49.8 Ϯ 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 Ϯ 0.21 vs. 5.31 Ϯ 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 IN THE FETUS, AN ACUTE DECREASE in arterial oxygen tension leads to cardiovascular responses, involving an elevation in blood pressure and redistribution of the cardiac output in favor of vital organs. In fetal lambs (10), fetal llamas (9), and chicken embryos (24, 25), increased levels of circulating catecholamines take part in this response. Early in gestation, the chromaffin cells in the primitive adrenal medulla are directly sensitive to low oxygen tension. Later in gestation, activation of efferent sympathetic nerves also contributes to the response (38). Antagonists of ␣-adrenoreceptors blunt the hypoxia-induced increase in fetal total peripheral resistance (9, 10, 25).Neurohumoral mechanisms have been proposed to be important regulators of blood flow in the hypoxemic fetus, but it remains to be established whether local and direct effects of decreased oxygen tension participate in the fetal cardiovascular response to hypoxemia. In previous studies, we have shown that chronic exposure to hypoxia affects both sympathetic innervation (34) and endothelium-dependent relaxation (33) of femoral arteries of the chicken embryo, but acute effects of hypoxia in isolated systemic arteries were not studied. Moreover, acute effects of low oxygen tension have been studied i...

Increased myogenic tone in 7-month-old adult male but not female offspring from rat dams exposed to hypoxia during pregnancy

“…Reduced nitric oxide modulation of vascular responses has also been found in fetal sheep exposed to chronic hypoxia at high altitude (33) and in embryonic and adult chickens after chronic exposure to hypoxia in ovo (42,43). Moreover, we recently demonstrated (55) decreased nitric oxide modulation of endothelium-dependent relaxation in 7-mo-old male offspring from dams exposed to hypoxia during pregnancy.…”

“…Exposure to chronic hypoxia in ovo results in reduced nitric oxide modulation of vascular responses in arteries from both embryonic and adult chickens (42,43). In mammals, the vascular effects of prenatal hypoxia have been examined primarily in the fetus (33,49) or the neonate (54).…”

Intermittent maternal hypoxia has an influence on regional expression of endothelial nitric oxide synthase in fetal arteries of rabbits

“…Conservation of brain and heart growth and reduced liver growth in fetuses after maternal hypoxia suggest that chronic maternal hypoxia caused changes in peripheral and/ or central artery resistance that redistributed cardiac output. The vascular resistance may depend on the balance between vasomotor influences of circulating catecholamines (9,10) and of endothelium-derived relaxing factors such as NO (10). Our study illustrates a differential effect of chronic intermittent maternal hypoxia on eNOS protein and mRNA expression in the common carotid and femoral artery segments of fetal rabbits.…”

“…Hypoxia alters the endothelial properties of fetal pulmonary (23), fetal carotid (16,17), cerebral (24), and femoral arteries (10,25,26). The effect of chronic hypoxia on fetal tissue eNOS gene expression is variable among different cell types.…”

“…It has been clearly demonstrated that one of the important fetal adaptations to either acute or sustained hypoxia is a redistribution of fetal cardiac output to ensure a preferential supply of nutrients to the brain and the heart and maintain their growth at the expense of the periphery (7,8). The redistribution of fetal cardiac output during hypoxia may partially depend on the balance between vasomotor influences of circulating catecholamines (9) and those of endotheliumderived relaxing factors such as nitric oxide (NO) (10).…”