Source:http://linkedlifedata.com/resource/pubmed/id/11273733
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2001-3-29
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pubmed:abstractText |
The effects of thyroid hormone (3,3',5-triiodo- L -thyronine, T3) on pacemaker activity were studied with electrophysiological and pharmacological approaches using spontaneously beating neonatal atrial myocytes cultured from 2-day-old rats. Treatment with T3 (10(-8)m) for 24-48 h led to a positive chronotropic effect. The beating rate of T3-treated cells was 244+/-19 beats/min and for control cells it was 122+/-10 beats/min (P<0.05). Action potentials were recorded and showed that the predominant effect of T3 was to increase the diastolic depolarization rate (99.5+/-9.8 in T3-treated group v 44.0+/-7.8 mV/s in untreated group). Some cells that exhibited pacemaker activity lacked a pacemaker current (I(f)) under voltage clamp conditions I(f)was recorded in 5 of 12 spontaneously active control cells and in 6 of 10 T3-treated cells. In those cells exhibiting the pacemaker current, the I(f)density was significantly larger in T3-treated cells (-7.9+/-2.6 pA/pF v-1.8+/-0.5 pA/pF in control). The L-type Ca2+ current density was similar in the two groups (at -7 mV, -7.5+/-1.5 in treated group v-8.6+/-1.0 pA/pF in control). In the presence of T3, the Na+-Ca2+ exchanger current (I(Na/Ca)) density was larger (e.g. at +60 mV, it was 4.8+/-0.5 v 3.5+/-0.2 pA/pF in control cells, P<0.05). As intracellular Ca2+ is extruded from the cell, the electrogenic Na+-Ca2+ exchanger causes a declining inward current, which may contribute to the pacemaker potential-this declining inward current was demonstrated using the action potential voltage clamp technique and was shown to be larger in T3-treated myocytes. Our data demonstrate that thyroid hormone enhances pacemaker activity and that this may be due in part to an increased Na+-Ca2+ exchanger activity.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-2828
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
33
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
811-24
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11273733-Action Potentials,
pubmed-meshheading:11273733-Animals,
pubmed-meshheading:11273733-Animals, Newborn,
pubmed-meshheading:11273733-Atrial Function,
pubmed-meshheading:11273733-Biological Clocks,
pubmed-meshheading:11273733-Calcium Channels, L-Type,
pubmed-meshheading:11273733-Cells, Cultured,
pubmed-meshheading:11273733-Electric Conductivity,
pubmed-meshheading:11273733-Electrophysiology,
pubmed-meshheading:11273733-Heart Atria,
pubmed-meshheading:11273733-Ions,
pubmed-meshheading:11273733-Myocardial Contraction,
pubmed-meshheading:11273733-Rats,
pubmed-meshheading:11273733-Sodium-Calcium Exchanger,
pubmed-meshheading:11273733-Triiodothyronine
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pubmed:year |
2001
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pubmed:articleTitle |
Thyroid hormone increases pacemaker activity in rat neonatal atrial myocytes.
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pubmed:affiliation |
Pediatric Cardiology, NYU School of Medicine, New York, NY 10016, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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