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Am J Physiol Lung Cell Mol Physiol (July 25, 2003). doi:10.1152/ajplung.00091.2003
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Submitted on April 1, 2003
Accepted on June 24, 2003

Chronic intrauterine pulmonary hypertension compromises fetal pulmonary artery smooth muscle cell oxygen sensing

Bradley C. Linden1*, Ernesto R. Resnik2, Kristine J. Hendrickson2, Jean M. Herron2, Timothy J. O'Connor2, and David N. Cornfield3

1 Department of Surgery, University of Minnesota, Minneapolis, MN, USA
2 Division of Pediatric Pulmonology and Critical Care Medicine, Department of Pediatrics, University of Minnesota, Minneapolis, MN, USA
3 Division of Pediatric Pulmonology and Critical Care Medicine, Department of Pediatrics, University of Minnesota, Minneapolis, MN, USA; Department of Surgery, University of Minnesota, Minneapolis, MN, USA; Department of Physiology, University of Minnesota, Minneapolis, MN, USA

* To whom correspondence should be addressed. E-mail: lind0186{at}umn.edu.

To test the hypothesis that chronic intrauterine pulmonary hypertension (PHTN) compromises pulmonary artery smooth muscle cell (PA SMC) O2 sensing, fluorescence microscopy was used to study the effect of an acute increase in O2 tension on the cytosolic calcium concentration ([Ca2+]i) of chronically hypoxic subconfluent monolayers of PA SMC in primary culture. PA SMC were derived from fetal lambs with PHTN due to intrauterine ligation of the ductus arteriosus. Acute normoxia decreased [Ca2+]i in control, but not PHTN PA SMC. In control PA SMC, [Ca2+]i increased after calcium-sensitive (KCa) and voltage-sensitive (Kv) K+ channel blockade, and decreased after diltiazem treatment. In PHTN PA SMC, KCa blockade had no effect, while Kv blockade and diltiazem increased [Ca2+]i. Inhibition of sarcoplasmic reticulum Ca2+ATP-ase activity caused a greater increase in [Ca2+]i in controls, compared to PHTN, PA SMC. Conversely, ryanodine caused a greater increase of [Ca2+]i in PHTN, compared to control, PA SMC. KCa channel mRNA is decreased and Kv channel mRNA is unchanged in PHTN PA SMC when compared to controls. We conclude that PHTN compromises PA SMC O2 sensing, alters intracellular calcium homeostasis, and changes the predominant ion channel that determines basal [Ca2+]i from KCa to Kv.




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