Referenced in: none

Automatically associated channels: BKβ

Title: Response of chicken ductus arteriosus to hypercarbic and normocarbic acidosis.

Authors: Rob M J Moonen, Pia Agren, Angel L Cogolludo, Francisco Perez Vizcaino, Eduardo Villamor

Journal, date & volume: Neonatology, 2010 Jun , 98, 47-56

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/20016222

Abstract
Changes in pH can have profound effects on vascular tone and reactivity, but their influence on the ductus arteriosus (DA) remains unknown.To analyzethe effects of hypercarbic and normocarbic acidosis in the reactivity of the chicken DA.DA rings from 19-day chicken fetuses (total incubation time, 21 days) were mounted in a wire myograph for isometric tension recording.In DA rings (pulmonary side) stimulated with O(2), norepinephrine (NE), KCl, or U46619, changes from control conditions (5% CO(2), 24 mM 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 mM NaHCO(3), pH 7.46) induced a transient contraction of the DA.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.