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Am J Physiol Lung Cell Mol Physiol 275: L1019-L1025, 1998;
1040-0605/98 $5.00
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Vol. 275, Issue 6, L1019-L1025, December 1998

A maturational shift in pulmonary K+ channels, from Ca2+ sensitive to voltage dependent

Helen L. Reeve1, E. Kenneth Weir2,3, Stephen L. Archer4, and David N. Cornfield5

Departments of 2 Medicine, 5 Pediatrics, and 1 Physiology, University of Minnesota, Minneapolis 55455; 3 Department of Cardiology, Veterans Affairs Medical Center, Minneapolis, Minnesota 55417; and 4 Department of Medicine, University of Alberta, Edmonton, Alberta, Canada T6G 2B7

The mechanism responsible for the abrupt decrease in resistance of the pulmonary circulation at birth may include changes in the activity of O2-sensitive K+ channels. We characterized the electrophysiological properties of fetal and adult ovine pulmonary arterial (PA) smooth muscle cells (SMCs) using conventional and amphotericin B-perforated patch-clamp techniques. Whole cell K+ currents of fetal PASMCs in hypoxia were small and characteristic of spontaneously transient outward currents. The average resting membrane potential (RMP) was -36 ± 3 mV and could be depolarized by charybdotoxin (100 nM) or tetraethylammonium chloride (5 mM; both blockers of Ca2+-dependent K+ channels) but not by 4-aminopyridine (4-AP; 1 mM; blocker of voltage-gated K+ channels) or glibenclamide (10 µM; blocker of ATP-dependent K+ channels). In hypoxia, chelation of intracellular Ca2+ by 5 mM 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid further reduced the amplitude of the whole cell K+ current and prevented spontaneously transient outward current activity. Under these conditions, the remaining current was partially inhibited by 1 mM 4-AP. K+ currents of fetal PASMCs maintained in normoxia were not significantly reduced by acute hypoxia. In normoxic adult PASMCs, whole cell K+ currents were large and RMP was -49 ± 3 mV. These 4-AP-sensitive K+ currents were partially inhibited by exposure to acute hypoxia. We conclude that the K+ channel regulating RMP in the ovine pulmonary circulation changes after birth from a Ca2+-dependent K+ channel to a voltage-dependent K+ channel. The maturational-dependent differences in the mechanism of the response to acute hypoxia may be due to this difference in K+ channels.

ion channels; hypoxia; pulmonary circulation; fetus; adult


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