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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
1998-2-3
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pubmed:abstractText |
We have tested the hypothesis that thyroid state may influence both the flow of cellular Ca2+ and the myofilament response to Ca2+ by effects on intracellular pH (pHi) and Na+ (Nai+). Single cardiac myocytes isolated from hypothyroid, euthyroid and hyperthyroid animals were loaded with fura-2/AM (Cai2+ probe), BCECF/AM (pHi probe) or SBFI/AM (Nai+ probe). Compared with hypothyroid animals, myocytes isolated from hyperthyroid rat hearts demonstrated a significant: (1) increase in extent of shortening; (2) decrease in the time to peak contraction; (3) increase in the peak amplitude of the fura-2 fluorescence ratio; (4) decrease in pHi (DeltapHi=0. 19+/-0.05); and (5) increase in Nai+ (DeltaNai+=2.88+/-0.55 mM). We have also compared pHi in Langendorff perfused hypo- and hyperthyroid rat hearts using NMR. We have found that hyperthyroid hearts are 0.15+/-0.03 pH units more acidic than hypothyroid hearts. Analysis of mRNA levels demonstrated that hyperthyroidism increased expression of both the Na+/Ca2+ exchanger and Na+/H+ antiporter, and decreased expression of Na+ channel mRNAs. These changes appear partially responsible for the observed changes in Nai+ and pHi. Our results provide the first evidence that changes in cardiac contractility associated with altered thyroid state not only involve effects on Ca2+, but may also involve changes in the response of the myofilaments to Cai2+mediated by altered pHi and Nai+.
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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/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Calcium Exchanger,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Hydrogen Antiporter,
http://linkedlifedata.com/resource/pubmed/chemical/Thyroid Hormones
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-2828
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 1997 Academic Press Limited.
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pubmed:issnType |
Print
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pubmed:volume |
29
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2653-63
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9344760-Animals,
pubmed-meshheading:9344760-Calcium,
pubmed-meshheading:9344760-Heart Ventricles,
pubmed-meshheading:9344760-Homeostasis,
pubmed-meshheading:9344760-Hydrogen-Ion Concentration,
pubmed-meshheading:9344760-Hyperthyroidism,
pubmed-meshheading:9344760-Hypothyroidism,
pubmed-meshheading:9344760-Male,
pubmed-meshheading:9344760-Myocardial Contraction,
pubmed-meshheading:9344760-Myocardium,
pubmed-meshheading:9344760-RNA, Messenger,
pubmed-meshheading:9344760-Rats,
pubmed-meshheading:9344760-Rats, Sprague-Dawley,
pubmed-meshheading:9344760-Sodium,
pubmed-meshheading:9344760-Sodium Channels,
pubmed-meshheading:9344760-Sodium-Calcium Exchanger,
pubmed-meshheading:9344760-Sodium-Hydrogen Antiporter,
pubmed-meshheading:9344760-Thyroid Gland,
pubmed-meshheading:9344760-Thyroid Hormones
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pubmed:year |
1997
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pubmed:articleTitle |
Changes in thyroid state affect pHi and Nai+ homeostasis in rat ventricular myocytes.
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pubmed:affiliation |
Dept of Physiology and Biophysics, College of Medicine, Chicago, IL 60612-7342, 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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