Document Detail


A maturational shift in pulmonary K+ channels, from Ca2+ sensitive to voltage dependent.
MedLine Citation:
PMID:  9843837     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 microM; 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.
Authors:
H L Reeve; E K Weir; S L Archer; D N Cornfield
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  275     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1998 Dec 
Date Detail:
Created Date:  1999-02-03     Completed Date:  1999-02-03     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  L1019-25     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Minnesota, Minneapolis 55455, Minnesota, USA.
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MeSH Terms
Descriptor/Qualifier:
Aging / physiology*
Animals
Anoxia / physiopathology
Calcium / physiology*
Electrophysiology
Fetus / physiology
Membrane Potentials / physiology
Muscle, Smooth, Vascular / cytology,  metabolism,  physiology
Patch-Clamp Techniques
Potassium Channels / physiology*
Pulmonary Artery / cytology,  metabolism*,  physiology
Sheep / embryology
Chemical
Reg. No./Substance:
0/Potassium Channels; 7440-70-2/Calcium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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