Changes in skeletal muscle SR Ca2+ pump in congestive heart failure due to myocardial infarction are prevented by angiotensin II blockade

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dc.contributor.authorShah, K
dc.contributor.authorGanguly, P
dc.contributor.authorNetticadan, T
dc.contributor.authorArneja, A
dc.contributor.authorDhalla, N
dc.date.accessioned2007-10-05T15:55:21Z
dc.date.available2007-10-05T15:55:21Z
dc.date.issued2004-07-31
dc.description.abstractIn order to understand the mechanisms of exercise intolerance and muscle fatigue, which are commonly observed in congestive heart failure, we studied sarcoplasmic reticulum (SR) Ca2+-transport in the hind-leg skeletal muscle of rats subjected to myocardial infarction (MI). Sham-operated animals were used for comparison. On one hand, the maximal velocities (Vmax) for both SR Ca2+-uptake and Ca2+-stimulated ATPase activities in skeletal muscle of rats at 8 weeks of MI were higher than those of controls. On the other hand, the Vmax values for both SR Ca2+-uptake and Ca2+-stimulated ATPase activities were decreased significantly at 16 weeks of MI when compared with controls. These alterations in Ca2+-transport activities were not associated with any change in the affinity (1/Ka) of the SR Ca2+-pump for Ca2+. Furthermore, the stimulation of SR Ca2+-stimulated ATPase activity by cyclic AMP-dependent protein kinase was not altered at 8 or 16 weeks of MI when compared with the respective control values. Treatment of 3-week infarcted animals with angiotensin-converting enzyme (ACE) inhibitors such as captopril, imidapril, and enalapril or an angiotensin receptor (AT(1)R) antagonist, losartan, for a period of 13 weeks not only attenuated changes in left ventricular function but also prevented defects in SR Ca2+-pump in skeletal muscle. These results indicate that the skeletal muscle SR Ca2+-transport is altered in a biphasic manner in heart failure due to MI. It is suggested that the initial increase in SR Ca2+-pump activity in skeletal muscle may be compensatory whereas the depression at late stages of MI may play a role in exercise intolerance and muscle fatigue in congestive heart failure. Furthermore, the improvements in the skeletal muscle SR Ca2+-transport by ACE inhibitors may be due to the decreased activity of renin-angiotensin system in congestive heart failure.en
dc.description.urihttps://www.ingentaconnect.com/content/cndscipub/cjpp/2004/00000082/00000007/art00002en_US
dc.format.extent113036 bytes
dc.format.mimetypeapplication/pdf
dc.identifier.citationCanadian Journal of Physiology and Pharmacology, JUL 2004;. 82(7):438-447.en
dc.identifier.doi10.1139/Y04-051
dc.identifier.urihttp://hdl.handle.net/1993/2896
dc.language.isoengen_US
dc.statusPeer revieweden
dc.subjectskeletal muscleen
dc.subjectsarcoplasmic reticulumen
dc.subjectCa2+-transporten
dc.subjectSR Ca2+-pumpen
dc.subjectcongestive heart failureen
dc.subjectrenin-angiotensin systemen
dc.subjectSARCOPLASMIC-RETICULUMen
dc.subjectGENE-EXPRESSIONen
dc.subjectDIABETIC CARDIOMYOPATHYen
dc.subjectEXERCISE INTOLERANCEen
dc.subjectCALCIUM-TRANSPORTen
dc.subjectBLOOD-FLOWen
dc.subjectRATSen
dc.subjectABNORMALITIESen
dc.subjectRELEASEen
dc.subjectFATIGUEen
dc.titleChanges in skeletal muscle SR Ca2+ pump in congestive heart failure due to myocardial infarction are prevented by angiotensin II blockadeen
dc.typejournal articleen_US
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