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1 Division of Pediatric Pulmonology and Critical Care Medicine, Department of Pediatrics, and 2 Department of Physiology, University of Minnesota, Minneapolis, Minnesota 55455; and 3 Department of Pediatrics, University of Nevada, Las Vegas, Nevada 89102
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.
ontogeny; smooth muscle cells; ion channel; cytosolic calcium
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