Pulmonary vascular response to normoxia and KCa channel activity is developmentally regulated

Michael Rhodes, Valerie A. Porter, Connie B. Saqueton, Jean M. Herron, Ernesto R. Resnik, David N. Cornfield

Research output: Contribution to journalArticlepeer-review

36 Scopus citations


To address developmental regulation of pulmonary vascular O2 sensing, we tested the hypotheses that 1) fetal but not adult pulmonary artery smooth muscle cells (PASMCs) can directly sense an acute increase in O2, 2) Ca2+-sensitive K+ (KCa) channel activity decreases with maturation, and 3) PASMC KCa channel expression decreases with maturation. We used fluorescence microscopy to confirm that fetal but not adult PASMCs are able to sense an acute increase in O2 tension. Acute normoxia induced a 22 ± 2% decrease in cytosolic Ca2+ concentration ([Ca2+]i) in fetal PASMCs and no change in [Ca2+]i in adult PASMCs (P < 0.01). The effects of K+ channel antagonists were studied on fetal and adult PASMC [Ca2+]i. Iberiotoxin (10-9 M) caused PASMC [Ca2+]i to increase by 694 ± 22% in the fetus and caused no change in adult PASMCs. KCa channel expression and mRNA levels in distal pulmonary arteries from fetal and adult sheep were examined. Both KCa channel protein and mRNA expression in the distal pulmonary vasculature decreased with maturation. We conclude that maturation-dependent changes in PASMC O2 sensing render the fetal PASMCs uniquely sensitive to an acute increase in O2 tension at a biologically critical time point.

Original languageEnglish (US)
Pages (from-to)L1250-L1257
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number6 24-6
StatePublished - 2001


  • Cytosolic calcium
  • Ion channel
  • Ontogeny
  • Smooth muscle cells


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