• Libraries
    • Log in to:
    View Item 
    •   MSpace Home
    • University of Manitoba Researchers
    • University of Manitoba Scholarship (login required)
    • View Item
    •   MSpace Home
    • University of Manitoba Researchers
    • University of Manitoba Scholarship (login required)
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

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

    View/Open
    Shah_Changes_in_skeletal.pdf (114.0Kb)
    Date
    2004-07-31
    Author
    Shah, K
    Ganguly, P
    Netticadan, T
    Arneja, A
    Dhalla, N
    Metadata
    Show full item record
    Abstract
    In 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.
    URI
    http://hdl.handle.net/1993/2896
    Collections
    • University of Manitoba Scholarship (login required) [171]

    DSpace software copyright © 2002-2016  DuraSpace
    Contact Us | Send Feedback
    Theme by 
    Atmire NV
     

     

    Browse

    All of MSpaceCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects

    My Account

    Login

    Statistics

    View Usage Statistics

    DSpace software copyright © 2002-2016  DuraSpace
    Contact Us | Send Feedback
    Theme by 
    Atmire NV