Response of Chicken Ductus Arteriosus to Hypercarbic and Normocarbic Acidosis

Rob M. J. Moonen, Pia Agren, Angel L. Cogolludo, Francisco Perez-Vizcaino, Eduardo Villamor*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

13 Citations (Web of Science)


Background: Changes in pH can have profound effects on vascular tone and reactivity, but their influence on the ductus arteriosus (DA) remains unknown. Objective: To analyze the effects of hypercarbic and normocarbic acidosis in the reactivity of the chicken DA. Methods: DA rings from 19-day chicken fetuses (total incubation time, 21 days) were mounted in a wire myograph for isometric tension recording. Results: In DA rings (pulmonary side) stimulated with O(2), norepinephrine (NE), KCl, or U46619, changes from control conditions (5% CO(2), 24 m M NaHCO(3), pH 7.4) to 7.5% CO(2) (pH 7.25) or 10% CO(2) (pH 7.14) induced a concentration-dependent relaxation that reached 43.0% (SD 21.3) of the O(2)(-), 28.6% (SD 23.1) of the NE-, 10.4% (SD 18.7) of the KCl-, and 6.8% (SD 12.6) of the U46619-induced contraction. Hypercarbic-acidosis-induced relaxation was impaired by the non-selective K(+) channel blocker tetraethylammonium or the BK(Ca) channel inhibitor iberiotoxin. Normocarbic acidosis (5% CO(2), 12 mM NaHCO(3), pH 7.13) induced transient relaxation of the DA, which was not affected by the presence of tetraethylammonium or iberiotoxin. Euhydric hypercarbia (10% CO(2), 48 m M NaHCO(3), pH 7.46) induced a transient contraction of the DA. Conclusions: Our results indicate that the chicken DA is very sensitive to changes in extracellular pH, and that stimulation of BK(Ca) channels may account for the ductal-relaxing effects of hypercarbic acidosis.
Original languageEnglish
Pages (from-to)47-56
Issue number1
Publication statusPublished - 2010


  • Ductus arteriosus
  • Acidosis
  • Permissive hypercapnia
  • Potassium channels

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