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Reactivity of chicken chorioallantoic arteries, avian homologue of human fetoplacental arteries
Linköping University, The Institute of Technology. Linköping University, Department of Physics, Chemistry and Biology, Zoology .
Linköping University, Department of Physics, Chemistry and Biology, Zoology . Linköping University, The Institute of Technology.
2010 (English)In: Journal of Physiology and Pharmacology, ISSN 0867-5910, Vol. 61, no 5, 619-628 p.Article in journal (Refereed) Published
Abstract [en]

The reactivity of human fetoplacental arteries is regulated by humoral and local factors of maternal and fetal origin. The chorioallantoic (CA) arteries of bird embryos are homologous to fetoplacental arteries and fulfill the same gas-exchange purpose without maternal influences, but their reactivity has not been studied in detail. In the present study we hypothesized that CA arteries would respond to vasoactive factors similarly to fetoplacental arteries and the response would change during development between maximal vascular CA expansion (15 of the 21 days incubation period) and prior to hatching. Therefore, we analyzed the reactivity of third order arteries (similar to 200 mu m) from the CA membrane of 15 and 19 day chicken embryos. CA arteries contracted in response to K+, the thromboxane A(2) mimetic U46619, endothelin-1, acetylcholine and acute hypoxia, but showed no reaction to alpha-adrenergic stimulation (phenylephrine). The nitric oxide donor sodium nitroprusside, the adenylyl cyclase agonist forskolin, and the beta-adrenergic agonist isoproterenol relaxed CA arteries precontracted with K+ or U46619. The contraction evoked by acetylcholine and the relaxations evoked by sodium nitroprusside and isoproterenol decreased with incubation age. In conclusion, CA arteries share many characteristics with human fetoplacental arteries, such as pronounced relaxation to beta-adrenergic stimuli and hypoxic vasoconstriction. Our study will be the foundation for future studies to explain disparate and common responses of the CA and fetoplacental vasculature.

Place, publisher, year, edition, pages
Polish Physiological Society , 2010. Vol. 61, no 5, 619-628 p.
Keyword [en]
beta-adrenergic agonist, chicken embryo, chorioallantoic membrane, hypoxic vasoconstriction, thromboxane A(2), vasoreactivity
National Category
Engineering and Technology
URN: urn:nbn:se:liu:diva-63392ISI: 000284790500013OAI: diva2:379154
Available from: 2010-12-17 Created: 2010-12-17 Last updated: 2011-02-04
In thesis
1. Cardiovascular beta-adrenergic signaling: Maturation and programming effects of hypoxia in a chicken model
Open this publication in new window or tab >>Cardiovascular beta-adrenergic signaling: Maturation and programming effects of hypoxia in a chicken model
2010 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Despite the importance of β-adrenergic receptors (βARs) in cardiovascular disease, not much is known about how prenatal hypoxia effects βAR signaling in the postnatal animal. Thus, the aim of this thesis was to characterize the pre- and postnatal maturation of the cardiovascular βARs and the effects of chronic prenatal hypoxia on βAR signaling in the embryo and adult animal using the chicken as experimental model.

βARs belong to the seven-transmembrane receptor family of G-protein coupled receptors and are crucial for cardiovascular development, growth and regulation. In the cardiovascular system there are two dominant  subtypes, β1AR and β2AR, whose main ligands are the biogenic catecholamines epinephrine and norepinephrine. When stimulated, βARs primarily couple to the stimulatory G-protein (Gas) that stimulates adenylyl cyclase to convert ATP to cAMP. cAMP increases ino- and chronotropy of the heart and causes relaxation of blood vessels. β2ARs also have the ability to switch to inhibitory G-protein (Gi) signaling that decreases the cAMP production. To protect the cardiovascular system from overstimulation, the βARs desensitize and downregulate in the case of prolonged elevation of catecholamines. This blunts the cardiovascular response and the mechanisms behind desensitization/downregulation, including the β2AR switch to Gi signaling, are closely linked to cardiovascular disease and are of immense importance in medical therapeutics.

Hypoxic stress releases catecholamines and thereby triggers βAR responses and desensitization/downregulation mechanisms. Hypoxia quite commonly occurs in utero and it is well known that prenatal insults, like malnutrition or hypoxia, are coupled to an increased risk of developing adult cardiovascular disease. This is referred to as developmental programming and constitutes an important and modern field of research.

In this thesis, I show that; 1) the developmental trajectory for organ growth, especially the heart, is affected by hypoxia, 2) chronic prenatal hypoxia causes cardiac embryonic βAR sensitization, but causes desensitization postnatally suggesting that there is a hypoxia-induced “programming” effect on adult β-adrenoceptor function, 3) the adult βAR desensitization following prenatal hypoxia is linked to a decrease in β1AR/β2AR ratio, a decrease in cAMP following βAR stimulation with isoproterenol and an increase in Gas, 4) the chorioallantoic (CA) membrane arteries display hypoxic vasoconstriction, but lack 8-adrenergic reactivity and 5) hypotension of the chronically hypoxic chicken embryo is linked to a potent βAR relaxation of the CA vasculature and an increased AR sensitivity of the systemic arteries with no changes in heart rate.

In conclusion, chronic prenatal hypoxia causes growth restriction, re-allocation and has programming effects on the βAR system in the adult. The latter indicates that the βAR system is an important factor in studying hypoxic developmental programming of adult cardiovascular disease.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2010. 48 p.
Linköping Studies in Science and Technology. Dissertations, ISSN 0345-7524 ; 1330
National Category
Natural Sciences
urn:nbn:se:liu:diva-65367 (URN)978-91.7393-352-0 (ISBN)
Public defence
2010-09-10, Planck, Hus E, Campus Valla, Linköpings universitet, Linköping, 09:15 (English)
Available from: 2011-02-04 Created: 2011-02-04 Last updated: 2012-11-19Bibliographically approved

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