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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2 Pt 1
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pubmed:dateCreated |
1998-3-23
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pubmed:abstractText |
In the present study, we investigated the effects of the naturally occurring hormone dehydroepiandrosterone (DHEA) on hypoxic pulmonary vasoconstriction (HPVC) in isolated ferret lungs and on K+ currents in isolated and cultured ferret pulmonary arterial smooth muscle cells (FPSMCs). Severe alveolar hypoxia (3% O2-5% CO2-92% N2) caused an initial increase in pulmonary arterial pressure (Ppa) that was followed by a reversal in pulmonary hypertension. Maintaining alveolar hypoxia caused a sustained secondary increase in Ppa. Pretreating the lungs with the K(+)-channel inhibitor tetraethylammonium (TEA) caused a small increase in baseline Ppa, potentiated HPVC, and prevented the reversal of HPVC during the sustained alveolar hypoxia. Treating the lungs with DHEA caused a near-complete reversal of HPVC in control lungs and in lungs that were pretreated with TEA. DHEA also reversed the KCl-induced increase in Ppa. In FPSMCs, DHEA caused an adenosine 3',5'-cyclic monophosphate- and guanosine 3',5'-cyclic monophosphate-independent increase in activity of the Ca(2+)-activated K+ (KCa) current. In a cell-attached configuration, DHEA caused a mean shift of -22 mV in the voltage-dependent activation of the KCa channel. We conclude that DHEA is a novel KCa-channel opener of the pulmonary vasculature.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Dehydroepiandrosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Large-Conductance...,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels...,
http://linkedlifedata.com/resource/pubmed/chemical/Tetraethylammonium
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
274
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
L186-95
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9486202-Animals,
pubmed-meshheading:9486202-Cell Hypoxia,
pubmed-meshheading:9486202-Cells, Cultured,
pubmed-meshheading:9486202-Cyclic AMP,
pubmed-meshheading:9486202-Cyclic GMP,
pubmed-meshheading:9486202-Dehydroepiandrosterone,
pubmed-meshheading:9486202-Ferrets,
pubmed-meshheading:9486202-Ion Channel Gating,
pubmed-meshheading:9486202-Large-Conductance Calcium-Activated Potassium Channels,
pubmed-meshheading:9486202-Muscle, Smooth, Vascular,
pubmed-meshheading:9486202-Potassium Channels,
pubmed-meshheading:9486202-Potassium Channels, Calcium-Activated,
pubmed-meshheading:9486202-Pulmonary Alveoli,
pubmed-meshheading:9486202-Pulmonary Circulation,
pubmed-meshheading:9486202-Pulmonary Wedge Pressure,
pubmed-meshheading:9486202-Tetraethylammonium,
pubmed-meshheading:9486202-Vasoconstriction
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pubmed:year |
1998
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pubmed:articleTitle |
Effect of dehydroepiandrosterone on hypoxic pulmonary vasoconstriction: a Ca(2+)-activated K(+)-channel opener.
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pubmed:affiliation |
Department of Internal Medicine, University of Utah Health Science Center, Salt Lake City 84132, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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