Linked Life Data

15717854

Source:http://linkedlifedata.com/resource/pubmed/id/15717854

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-12-14
pubmed:abstractText
The inotropic effects of insulin in the rat heart are still incompletely understood. In this study, the effects of insulin on cardiac contraction were studied in right ventricular papillary muscles from both control rats and rats with chronic diabetes (lasting 16 weeks). Diabetes was induced by the application of streptozotocin (STZ) and the development of diabetes was documented by increased levels of blood glucose, by reduction in body weight and by decreased plasma concentrations of insulin. The contraction was significantly smaller in diabetic rats. Insulin (80 IU/l) reduced the contraction force in both control and diabetic groups. The post-rest potentiation of contraction was not influenced by insulin in control rats, but insulin increased it in diabetic rats. The negative inotropic effect of insulin was preserved in the presence of cyclopiazonic acid (3 micromol/l), a blocker of sarcoplasmic reticulum (SR) Ca2+ pump, in both control and diabetic groups. In contrast, the negative inotropic effect of insulin was completely prevented in the presence of nifedipine (3 micromol/l), a blocker of L-type Ca2+ current. We conclude that insulin exerts a significant negative inotropic effect in rat myocardium, both control and diabetic. This effect is probably related to processes of SR Ca2+ release triggering, whereas SR Ca2+ loading is not involved.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0862-8408
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
661-70
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Negative inotropic effect of insulin in papillary muscles from control and diabetic rats.
pubmed:affiliation
Department of Physiology, Faculty of Medicine, Charles University, Lidická 1, 301 66 Plzen, Czech Republic. jitka.sviglerova@lfp.cuni.cz
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't