Linked Life Data

1694410

Source:http://linkedlifedata.com/resource/pubmed/id/1694410

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6 Pt 2
pubmed:dateCreated
1990-8-2
pubmed:abstractText
In rat heart, the maximum velocity of shortening is decreased in response to chronic pressure overload. This is in part explained by an isomyosin shift, but several arguments suggest changes in membrane proteins. Inotropic response to calcium channel modifiers and to external calcium were simultaneously determined to explore this possibility. Left ventricular hypertrophy was induced by abdominal aortic stenosis and after 4-5 wk the left ventricular-to-body weight ratio increased by 61%. The effects of BAY K 8644 (10(-9) to 10(-6) M), a calcium channel activator, nifedipine (10(-9) to 10(-7) M), and external calcium (0.25-2.50 mM) were studied on isolated hearts at a coronary flow of 20 ml.min-1.g of left ventricle-1. The inotropic response (in percent changes in developed pressure and in dP/dtmax) was unmodified in the hypertrophied hearts. This work is in agreement with previous findings that both the total number of dihydropyridine binding sites and the peak magnitude of calcium current increase in proportion to the degree of hypertrophy. It suggests that the slowing of velocity could not be explained by a decreased number of Ca2+ channels but may more likely reflect modifications of the sarcomeres or sarcoplasmic reticulum.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
258
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1727-34
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Normal responsiveness to external Ca and to Ca-channel modifying agents in hypertrophied rat heart.
pubmed:affiliation
Institut National de la Santé et de Recherche Médicale (INSERM) U127, Hôpital, Paris, France.
pubmed:publicationType
Journal Article, In Vitro