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Am J Physiol Lung Cell Mol Physiol 283: L1103-L1109, 2002. First published August 2, 2002; doi:10.1152/ajplung.00100.2002
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Vol. 283, Issue 5, L1103-L1109, November 2002

Contribution of the KCa channel to membrane potential and O2 sensitivity is decreased in an ovine PPHN model

Andrea Olschewski1, Zhigang Hong2, Bradley C. Linden3, Valerie A. Porter4, E. Kenneth Weir2,5, and David N. Cornfield4,6

1 Department of Anesthesiology, Justus Liebig University, 35392 Giessen, Germany; 2 Veterans Affairs Medical Center, Minneapolis 55417; and 4 Department of Pediatrics, Division of Pediatric Pulmonology and Critical Care, Departments of 3 Surgery, 6 Physiology, and 5 Medicine, University of Minnesota Medical School, Minneapolis, Minnesota 55455

Ca2+-sensitive K+ (KCa) channels play an important role in mediating perinatal pulmonary vasodilation. We hypothesized that lung KCa channel function may be decreased in persistent pulmonary hypertension of the newborn (PPHN). To test this hypothesis, pulmonary artery smooth muscle cells (PASMC) were isolated from fetal lambs with severe pulmonary hypertension induced by ligation of the ductus arteriosus in fetal lambs at 125-128 days gestation. Fetal lambs were killed after pulmonary hypertension had been maintained for at least 7 days. Age-matched, sham-operated animals were used as controls. PASMC K+ currents and membrane potentials were recorded using amphotericin B-perforated patch-clamp techniques. The increase in whole cell current normally seen in response to normoxia was decreased (333.9 ± 63.6% in control vs. 133.1 ± 16.0% in hypertensive fetuses). The contribution of the KCa channel to the whole cell current was diminished in hypertensive, compared with control, fetal PASMC. In PASMC from hypertensive fetuses, a change from hypoxia to normoxia caused no change in membrane potential compared with a -14.6 ± 2.8 mV decrease in membrane potential in PASMC from control animals. In PASMC from animals with pulmonary hypertension, 4-aminopyridine (4-AP) caused a larger depolarization than iberiotoxin, whereas in PASMC from control animals, iberiotoxin caused a larger depolarization than 4-AP. These data confirm the hypothesis that the contribution of the KCa channel to membrane potential and O2 sensitivity is decreased in an ovine model of PPHN, and this may contribute to the abnormal perinatal pulmonary vasoreactivity associated with PPHN.

pulmonary hypertension; fetus; oxygen sensing; persistent pulmonary hypertension of the newborn; Ca2+-sensitive K+ channel


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