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Articles in PresS, published online ahead of print August 2, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00100.2002
Submitted on April 4, 2002
Accepted on July 8, 2002
1 Department of Anesthesiology, Justus-Leibig- University, Giessen, Germany
2 Department of Medicine, Veteran's Administration Medical Center, Minneapolis, MN, USA
3 Department of Surgery, University of Minnesota Medical School, Minneapolis, MN, USA
4 Department of Pediatrics, University of Minnesota Medical School, Minneapolis, MN, USA; Physiology, rsity of Minnesota, Minneapolis, MN, USA
5 Department of Medicine, University of Minnesota, Minneapolis, MN, USA; Department of Medicine, Veteran's Administration Medical Center, Minneapolis, MN, USA; Physiology, rsity of Minnesota, Minneapolis, MN, USA
6 Department of Pediatrics, University of Minnesota Medical School, Minneapolis, MN, USA; Department of Physiology, University of Minnesota, Minneapolis, MN, USA
* To whom correspondence should be addressed. E-mail: cornf001{at}tc.umn.edu.
Calcium-sensitive potassium (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 sacrificed 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 to control, fetal PASMC. In PASMC from hypertensive fetuses, a change from hypoxia to normoxia caused no change in membrane potential, compared to -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, while in PASMC from control animals, iberiotoxin caused a larger depolarization than 4-AP. This data confirms the hypothesis that the contribution of the KCa channel to membrane potential and oxygen sensitivity is decreased in an ovine model of PPHN and this may contribute to the abnormal perinatal pulmonary vasoreactivity associated with PPHN.
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