Heart glycogen content and isoprenaline-induced myocardial lesions
Language English Country Netherlands Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
8974050
DOI
10.1007/bf00408651
Knihovny.cz E-resources
- MeSH
- Adenylyl Cyclases metabolism MeSH
- Adrenergic beta-Agonists pharmacology MeSH
- Glycogen metabolism MeSH
- Guanylyl Imidodiphosphate pharmacology MeSH
- Isoproterenol pharmacology MeSH
- Colforsin pharmacology MeSH
- Rats MeSH
- Myocardium metabolism MeSH
- Rats, Wistar MeSH
- Propranolol pharmacology MeSH
- Heart drug effects MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adenylyl Cyclases MeSH
- Adrenergic beta-Agonists MeSH
- Glycogen MeSH
- Guanylyl Imidodiphosphate MeSH
- Isoproterenol MeSH
- Colforsin MeSH
- Propranolol MeSH
The role of glycogen content in the heart for the development of isoprenaline-induced myocardial lesions (IML) was studied in Wistar rats and in two inbred rat strains: In IR rats (resistant to the development of IML) and in IS rats (sensitive to IML development). Glycogen content in the heart can be dramatically lowered or increased by various interventions. IML develop during the period of very low heart glycogen content (about 0.6 mg.g-1) induced by isoprenaline administration. In animals with increased resistance to IML, either due to genetic factors or induced by isoprenaline pretreatment a high glycogen content in the heart is found (up to 7.5 mg.g-1). The increase of resistance to IML development and increased glycogen content induced by isoprenaline pretreatment were accompanied by lower basal or ISO-, guanylylimidodiphosphate- (Gpp/NH/p) and forskolin-stimulated activities of adenylyl cyclase. On the other hand, these parameters did not differ between IR and IS rats in spite of the presence of significant differences in the resistance to the development of IML and in heart glycogen content in these two rats strains. These results suggest that genetically determined differences between two inbred rat strains in the resistance of the heart to the development of IML and in the heart glycogen content are caused by factors which are independent of the receptor-adenylyl cyclase complex and are therefore different from those involved in the increase of resistance and glycogen content due to isoprenaline pretreatment.
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