Vascular reactivity in intrapulmonary arteries of chicken embryos during transition to ex ovo life

Villamor, Eduardo; Ruijtenbeek, K.; Pulgar, Víctor M.; Mey, Jo G. R. De; Blanco, Carlos E.

doi:10.1152/ajpregu.00369.2001

Cited by 40 publications

(57 citation statements)

References 51 publications

(81 reference statements)

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“…Mediators, like catecholamines Hassanzadeh et al, 1997aHassanzadeh et al, , 2001Hassanzadeh et al, , 2002, endothelin-1 (Villamor et al, 2002;Odom et al, 2004), methylglyoxal (Khajali and Fahimi, 2010;Khajali and Wideman, 2011) and serotonin (Chapman and Wideman, 2002;Kluess et al, 2012) play a major role in accelerating of pulmonary hypertension that may lead to ascites in broiler chickens (Hassanzadeh et al, 1997a, b;Wideman et al, 2013).…”

Section: B Mediators Contributed To Pulmonary Arterial Hypertensionmentioning

confidence: 99%

“…Lefkowitz et al (1984) and Cohen et al (1984) reported that the constriction of smooth muscles of the vascular system was a consequence of an adrenergic stimulation due to catecholamine hormones. So, intravenously administered epinephrine elicits immediate pulmonary vasoconstriction accompanied by pulmonary hypertension (Wideman, 1999;Villamor et al, 2002;Lorenzoni and RuizFeria, 2006;Ruiz-Feria, 2009;Bautista-Ortega and RuizFeria, 2010).…”

Section: B Mediators Contributed To Pulmonary Arterial Hypertensionmentioning

confidence: 99%

“…In broilers, endothelin-1 elicits dose-dependent constriction of pulmonary arteries that can be modulated by nitric oxide (Martinez-Lemus et al, 2003;Villamor et al, 2002;Odom et al, 2004). Repeated intravenous injections of endothelin-1 triggered pulmonary arterial hypertension in broiler chickens (Zhou et al, 2008).…”

Section: B Mediators Contributed To Pulmonary Arterial Hypertensionmentioning

confidence: 99%

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Ascites Syndrome in Broiler Chickens: A Review on the Aspect of Endogenous and Exogenous Factors Interactions

et al. 2014

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Increasing susceptibility of broiler chickens to ascites syndrome has coincided with a continuing genetic and nutritional improvement in their feed efficiency and growth rate. Imbalance between oxygen supply and the oxygen required to sustain rapid growth rates and high food efficiencies is believed to be the primary cause of ascites. This imbalance is caused by exogenous and/or endogenous factors.Selection in fast growth broilers, have also resulted in the development of birds with changed anatomical, physiological, metabolic and hematological parameters including thyroid hormone activity, partial pressure of O 2 and carbon dioxide in venous blood, cardiac β-adrenergic receptors and hematocrit levels that coincide with susceptibility to ascites in broiler chickens. Observations to date have indicated that the structural or endocrine changes are often linked with ascites susceptibility and may be influenced during the early stages of development, embryogenesis and incubation. In this review, particular attention is paid to the interactions between endogenous and exogenous factors as predisposing factors for development of ascites syndrome. Additionally, preventive management procedures like different lighting schedules, feed restriction protocols and supplementation of feed with antioxidants which reduce the incidence of ascites in broiler chickens are highlighted.

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Section: B Mediators Contributed To Pulmonary Arterial Hypertensionmentioning

confidence: 99%

Section: B Mediators Contributed To Pulmonary Arterial Hypertensionmentioning

confidence: 99%

Section: B Mediators Contributed To Pulmonary Arterial Hypertensionmentioning

confidence: 99%

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Ascites Syndrome in Broiler Chickens: A Review on the Aspect of Endogenous and Exogenous Factors Interactions

et al. 2014

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“…The Wnal pH was 7.38-7.42 and pCO 2 was 4.6-5.6 kPa in all solutions. Each DA was stretched to its individual optimal lumen diameter, i.e., the diameter at which it developed the strongest contractile response to 62.5 mM K + , using a diameter-tension protocol as previously described (Agren et al 2007;Villamor et al 2002). During the Wrst phase of stabilization and determination of optimal diameter, DA rings were maintained in KRB buVer with a pO 2 of »3 kPa.…”

Section: Recording Of Arterial Reactivitymentioning

confidence: 99%

Developmental changes in the effects of prostaglandin E2 in the chicken ductus arteriosus

et al. 2008

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Prostaglandin E 2 (PGE 2 ) is the major vasodilator prostanoid of the mammalian ductus arteriosus (DA). In the present study we analyzed the response of isolated DA rings from 15-, 19-and 21-day-old chicken embryos to PGE 2 and other vascular smooth muscle relaxing agents acting through the cyclic AMP signaling pathway. PGE 2 exhibited a relaxant response in the 15-day DA, but not in the 19-and 21-day DA. Moreover, high concentrations of PGE 2 (¸3 M in 15-day and ¸1 M in 19-day and 21-day DA) induced contraction of the chicken DA. The presence of the TP receptor antagonist SQ29,548, unmasked a relaxant eVect of PGE 2 in the 19-and 21-day DA and increased the relaxation induced by PGE 2 in the 15-day DA. The presence of the EP receptor antagonist AH6809 abolished PGE 2 -mediated relaxation. The relaxant responses induced by PGE 2 and the -adrenoceptor agonist isoproterenol, but not those elicited by the adenylate cyclase activator forskolin or the phosphodiesterase 3 inhibitor milrinone, decreased with maturation. High oxygen concentrations (95%) decreased the relaxation to PGE 2 . The relaxing potency and eYcacy of isoproterenol and milrinone were higher in the pulmonary than in the aortic side of the DA, whereas no regional diVerences were found in the response to PGE 2 . We conclude that, in contrast to the mammalian situation, PGE 2 is a weak relaxant agent of the chicken DA and, with advancing incubation, it even stimulates TP vasoconstrictive receptors.

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“…Chicken embryos have a mammalian-like circulation, with an extraembryonic circuit involved in the gas exchange (the chorioallantois), analogous to the placenta, and they maintain bilaterally developed DA (3). During the past few years, our group has analyzed developmental changes in reactivity of chicken embryo systemic and pulmonary arteries (26,38,51,52). In the present study, we hypothesized that the responsiveness of the chicken embryo DA to O 2 and other vasoconstrictors is developmentally regulated.…”

mentioning

confidence: 97%

Ontogeny of chicken ductus arteriosus response to oxygen and vasoconstrictors

Ågren¹,

Cogolludo²,

Kessels³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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108

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The present study aimed to characterize the contractile reactivity of the chicken ductus arteriosus (DA) from the last stage of prenatal development and throughout the perinatal period. Isolated DA rings from 15-day, noninternally-pipped 19-day, and externally-pipped 21-day embryos were studied using myograph techniques. On embryonic day 15, the chicken DA did not respond to O 2 (0 to 21%), norepinephrine (NE), or phenylephrine (Phe) but contracted in response to high-K ϩ solution, the inhibitor of voltage-gated channels 4-aminopyridine, U-46619, and endothelin (ET)-1. These responses increased with advancing incubation age. Contractile responses to O 2, NE, and Phe were present in the 19-and 21-day embryo. Oxygen-induced contraction was restricted to the pulmonary side of the DA and was augmented by the nitric oxide synthase inhibitor N -nitro-L-arginine methyl ester and the soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and reduced by the peptidic ET A and ETB-receptor antagonist PD-142,893. Transmural electrical stimulation of nerves, the nonselective cyclooxygenase (COX) inhibitor indomethacin, the COX-1 inhibitor valeryl salicylate, the COX-2 inhibitor nimesulide, the inhibitor of ATP-sensitive K ϩ channels glibenclamide, and the inhibitor of Ca 2ϩ -activated K ϩ channels tetraethylammonium did not cause contraction of the DA rings at any age. We conclude that transition to ex ovo life is accompanied by dramatic changes in chicken DA reactivity. At 0.7 incubation, excitation-contraction and pharmacomechanical coupling for several contractile agonists are already present, whereas the constrictor effects of O 2 and cathecolamines appear later in development and are located in the pulmonary side of the DA. ductus arteriosus; chicken embryo; potassium channels; oxygen sensing; cathecolamines.THE DUCTUS ARTERIOSUS (DA) is a vessel that connects the pulmonary artery to the aorta and provides, during the fetal life, a pulmonary-to-systemic diversion that shunts more than half of the right ventricle output away from the nonventilated lungs into the systemic circulation (43, 47). The main factors maintaining patency of the DA in utero are low O 2 tension, high levels of circulating PGE 2 , and locally produced PGE 2 and PGI 2 (24, 43). Failure of DA closure after birth is a common complication of premature delivery that is still presenting challenges in terms of diagnosis, assessment, and treatment options (43).Although the isolated DA is sensitive to a wide range of contractile agonists, the major factor actively stimulating contraction at birth is increasing O 2 tension, which has a profound effect on the DA, both directly and by modulating its response to vasodilators and vasoconstrictors (43). To constrict properly after birth, the DA prepares itself for this specific task from a quite early onset during development (3). This preparation is reflected by changes in responsiveness with advancing gestational age. These have been extensively characterized in numerous mammalian specie...

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Vascular reactivity in intrapulmonary arteries of chicken embryos during transition to ex ovo life

Cited by 40 publications

References 51 publications

Ascites Syndrome in Broiler Chickens: A Review on the Aspect of Endogenous and Exogenous Factors Interactions

Ascites Syndrome in Broiler Chickens: A Review on the Aspect of Endogenous and Exogenous Factors Interactions

Developmental changes in the effects of prostaglandin E2 in the chicken ductus arteriosus

Ontogeny of chicken ductus arteriosus response to oxygen and vasoconstrictors

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