Linked Life Data

9559416

Source:http://linkedlifedata.com/resource/pubmed/id/9559416

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-6-16
pubmed:abstractText
To investigate Ca2+ handling in compensated hypertrophied cardiomyocytes, we measured Ca2+ transients and contraction of hypertrophied rat left ventricular myocytes induced by aortic constriction (AC). The fluorescence ratio (I405/I480) after indo-1/AM loading and circumferential length were simultaneously measured in isolated myocytes. The amplitude of Ca2+ transients (Ca-Amp) was higher in rats with AC than in sham-operated rats (Sham) (0.25 +/- 0.08 vs 0.17 +/- 0.05). There was a positive correlation between Ca-Amp and fractional shortening (FS) in both AC and Sham rats, whereas the ratio of FS/Ca-Amp was smaller in AC rats. These observations suggest that compensated hypertrophied cardiomyocytes exhibit an adaptive increase in Ca-Amp, associated with reduced myofilament responsiveness to an increase in Ca2+. Isoproterenol and forskolin increased Ca-Amp and FS, and decreased time to 50% decline of Ca2+ transients. Although myocytes from AC rats exhibited reduced responsiveness to isoproterenol, responses to forskolin did not differ between the 2 groups. The reduced beta-adrenergic response in Ca2+ handling was probably due to altered beta-adrenoceptor numbers, G-protein function and/or their coupling process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0047-1828
pubmed:author
pubmed:issnType
Print
pubmed:volume
62
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
36-46
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Altered calcium handling in compensated hypertrophied rat cardiomyocytes induced by pressure overload.
pubmed:affiliation
Third Department of Medicine, Kurume University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't