Source:http://linkedlifedata.com/resource/pubmed/id/10409108
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1 Pt 1
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pubmed:dateCreated |
1999-8-18
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pubmed:abstractText |
These experiments were performed to determine the effects of reducing Ca(2+) influx (Ca(in)) on K(+) currents (I(K)) in myocytes from rat small mesenteric arteries by 1) adding external Cd(2+) or 2) lowering external Ca(2+) to 0.2 mM. When measured from a holding potential (HP) of -20 mV (I(K20)), decreasing Ca(in) decreased I(K) at voltages where it was active (>0 mV). When measured from a HP of -60 mV (I(K60)), decreasing Ca(in) increased I(K) at voltages between -30 and +20 mV but decreased I(K) at voltages above +40 mV. Difference currents (DeltaI(K)) were determined by digital subtraction of currents recorded under control conditions from those obtained when Ca(in) was decreased. At test voltages up to 0 mV, DeltaI(K60) exhibited kinetics similar to control I(K60), with rapid activation to a peak followed by slow inactivation. At 0 mV, peak DeltaI(K60) averaged 75 +/- 13 pA (n = 8) with Cd(2+) and 120 +/- 20 pA (n = 9) with low Ca(2+) concentration. At test voltages from 0 to +60 mV, DeltaI(K60) always had an early positive peak phase, but its apparent "inactivation" increased with voltage and its steady value became negative above +20 mV. At +60 mV, the initial peak DeltaI(K60) averaged 115 +/- 18 pA with Cd(2+) and 187 +/- 34 pA with low Ca(2+). With 10 mM pipette BAPTA, Cd(2+) produced a small inhibition of I(K20) but still increased I(K60) between -30 and +10 mV. In Ca(2+)-free external solution, Cd(2+) only decreased both I(K20) and I(K60). In the presence of iberiotoxin (100 nM) to inhibit Ca(2+)-activated K(+) channels (K(Ca)), Cd(2+) increased I(K60) at all voltages positive to -30 mV while BAY K 8644 (1 microM) decreased I(K60). These results suggest that Ca(in), through L-type Ca(2+) channels and perhaps other pathways, increases K(Ca) (i.e., I(K20)) and decreases voltage-dependent K(+) currents in this tissue. This effect could contribute to membrane depolarization and force maintenance.
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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/1,2-bis(2-aminophenoxy)ethane-N,N,N'...,
http://linkedlifedata.com/resource/pubmed/chemical/3-Pyridinecarboxylic acid...,
http://linkedlifedata.com/resource/pubmed/chemical/Cadmium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Chelating Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/iberiotoxin
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
277
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C51-63
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10409108-3-Pyridinecarboxylic acid...,
pubmed-meshheading:10409108-Animals,
pubmed-meshheading:10409108-Cadmium,
pubmed-meshheading:10409108-Calcium,
pubmed-meshheading:10409108-Calcium Channel Agonists,
pubmed-meshheading:10409108-Chelating Agents,
pubmed-meshheading:10409108-Egtazic Acid,
pubmed-meshheading:10409108-Electric Conductivity,
pubmed-meshheading:10409108-Electrophysiology,
pubmed-meshheading:10409108-Mesenteric Arteries,
pubmed-meshheading:10409108-Muscle, Smooth, Vascular,
pubmed-meshheading:10409108-Patch-Clamp Techniques,
pubmed-meshheading:10409108-Peptides,
pubmed-meshheading:10409108-Potassium,
pubmed-meshheading:10409108-Rats
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pubmed:year |
1999
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pubmed:articleTitle |
Ca(2+) influx inhibits voltage-dependent and augments Ca(2+)-dependent K(+) currents in arterial myocytes.
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pubmed:affiliation |
Department of Physiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6085, USA. rcox@mail.med.upenn.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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