Vascular reactivity in intrapulmonary arteries of chicken embryos during transition to ex ovo life.
The present study aimed to characterize pulmonary vascular reactivity in the chicken embryo from the last stage of prenatal development and throughout the perinatal period. Isolated intrapulmonary arteries from non-internally pipped embryos at 19 days of incubation and from internally and externally pipped embryos at 21 days of incubation were studied. Arterial diameter and contractile responses to KCl, endothelin-1, and U-46619 increased with incubation but were unaffected by external pipping. In contrast, the contractions induced by norepinephrine, phenylephrine, and electric field stimulation decreased with development. No developmental changes were observed in endothelium-dependent [acetylcholine (ACh) and cyclopiazonic acid] or endothelium-independent [sodium nitroprusside (SNP)] relaxation. These relaxations were abolished by the soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one. Endothelium-dependent relaxation was unaffected by blockade of cyclooxygenase or heme oxygenase but was significantly reduced by nitric oxide (NO) synthase inhibitors. Reduction of O2 concentration from 95 to 5% produced a marked reduction in ACh and SNP-induced relaxations. Chicken embryo pulmonary arteries show a marked endothelium-dependent relaxation that is unaffected by transition to ex ovo life. Endothelium-derived NO seems to be the main mediator responsible for this relaxation.
Villamor
Eduardo
E
Department of Pediatrics, University Hospital Maastricht, Research Institute Growth and Development, University of Maastricht, 6202 AZ Maastricht, The Netherlands. eiv@skin.azm.nl
Ruijtenbeek
Karin
K
Pulgar
Victor
V
De Mey
Jo G R
JG
Blanco
Carlos E
CE
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D002642:Chick Embryo / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D066298:In Vitro Techniques; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010069:Oxadiazoles / Q000494:pharmacology; D011651:Pulmonary Artery / Q000187:drug effects / Q000196:embryology* / Q000502:physiology*; D011810:Quinoxalines / Q000494:pharmacology; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology; D014666:Vasomotor System / Q000196:embryology* / Q000502:physiology*
C095284:1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one; D004791:Enzyme Inhibitors; D010069:Oxadiazoles; D011810:Quinoxalines; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester