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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2000-12-1
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pubmed:abstractText |
Large-conductance potassium (BK) channels in vascular smooth muscle cells (VSMCs) sense both changes in membrane potential and in intracellular Ca(2+) concentration. BK channels may serve as negative feedback regulators of vascular tone by linking membrane depolarization and local increases in intracellular Ca(2+) concentration (Ca(2+) sparks) to repolarizing spontaneous transient outward K(+) currents (STOCs). BK channels are composed of channel-forming BKalpha and auxiliary BKbeta1 subunits, which confer to BK channels an increased sensitivity for changes in membrane potential and Ca(2+). To assess the in vivo functions of this ss subunit, mice with a disrupted BKbeta1 gene were generated. Cerebral artery VSMCs from BKbeta1 -/- mice generated Ca(2+) sparks of normal amplitude and frequency, but STOC frequencies were largely reduced at physiological membrane potentials. Our results indicate that BKbeta1 -/- mice have an abnormal Ca(2+) spark/STOC coupling that is shifted to more depolarized potentials. Thoracic aortic rings from BKbeta1 -/- mice responded to agonist and elevated KCl with a increased contractility. BKbeta1 -/- mice had higher systemic blood pressure than BKbeta1 +/+ mice but responded normally to alpha(1)-adrenergic vasoconstriction and nitric oxide-mediated vasodilation. We propose that the elevated blood pressure in BKbeta1 -/- mice serves to normalize Ca(2+) spark/STOC coupling for regulating myogenic tone. The full text of this article is available at http://www.circresaha.org.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1524-4571
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
24
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pubmed:volume |
87
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
E53-60
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11090555-Animals,
pubmed-meshheading:11090555-Calcium Signaling,
pubmed-meshheading:11090555-Cells, Cultured,
pubmed-meshheading:11090555-Cerebral Arteries,
pubmed-meshheading:11090555-Female,
pubmed-meshheading:11090555-Gene Targeting,
pubmed-meshheading:11090555-Homozygote,
pubmed-meshheading:11090555-Hypertension,
pubmed-meshheading:11090555-Large-Conductance Calcium-Activated Potassium Channels,
pubmed-meshheading:11090555-Male,
pubmed-meshheading:11090555-Membrane Potentials,
pubmed-meshheading:11090555-Mice,
pubmed-meshheading:11090555-Mice, Inbred C57BL,
pubmed-meshheading:11090555-Mice, Knockout,
pubmed-meshheading:11090555-Muscle, Smooth, Vascular,
pubmed-meshheading:11090555-Potassium,
pubmed-meshheading:11090555-Potassium Channels,
pubmed-meshheading:11090555-Potassium Channels, Calcium-Activated,
pubmed-meshheading:11090555-Potassium Chloride,
pubmed-meshheading:11090555-Protein Subunits,
pubmed-meshheading:11090555-RNA, Messenger,
pubmed-meshheading:11090555-Sequence Analysis, DNA,
pubmed-meshheading:11090555-Signal Transduction,
pubmed-meshheading:11090555-Vasoconstriction,
pubmed-meshheading:11090555-Vasodilator Agents
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pubmed:year |
2000
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pubmed:articleTitle |
Mice with disrupted BK channel beta1 subunit gene feature abnormal Ca(2+) spark/STOC coupling and elevated blood pressure.
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pubmed:affiliation |
Institut für Neurale Signalverarbeitung, ZMNH, Universität Hamburg, Hamburg, Germany.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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