Heart glycogen content and isoprenaline-induced myocardial lesions
Jazyk angličtina Země Nizozemsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
8974050
DOI
10.1007/bf00408651
Knihovny.cz E-zdroje
- MeSH
- adenylátcyklasy metabolismus MeSH
- agonisté adrenergních beta-receptorů farmakologie MeSH
- glykogen metabolismus MeSH
- guanylylimidodifosfát farmakologie MeSH
- isoprenalin farmakologie MeSH
- kolforsin farmakologie MeSH
- krysa rodu Rattus MeSH
- myokard metabolismus MeSH
- potkani Wistar MeSH
- propranolol farmakologie MeSH
- srdce účinky léků MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- adenylátcyklasy MeSH
- agonisté adrenergních beta-receptorů MeSH
- glykogen MeSH
- guanylylimidodifosfát MeSH
- isoprenalin MeSH
- kolforsin 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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