scholarly journals SKELETAL MUSCLE CONTRACTILE APPARATUS AND SARCOPLASMIC RETICULUM FUNCTION IN CONGESTIVE HEART FAILURE 839

1996 ◽  
Vol 28 (Supplement) ◽  
pp. 141
Author(s):  
C. W. Ward ◽  
J. H. Williams
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Congestive Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Contractile Apparatus ◽  
Muscle Contractile

Skeletal Muscle Sarcoplasmic Reticulum Ca 2+ -ATPase Gene Expression in Congestive Heart Failure

1997 ◽  
Vol 81 (5) ◽  
pp. 703-710 ◽  
Author(s):  
David G. Peters ◽  
Heather L. Mitchell ◽  
Sylvia A. McCune ◽  
Sonhee Park ◽  
Jay H. Williams ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Congestive Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Atpase Gene

Functional aspects of skeletal muscle contractile apparatus and sarcoplasmic reticulum after fatigue

1998 ◽  
Vol 85 (2) ◽  
pp. 619-626 ◽  
Author(s):  
Jay H. Williams ◽  
Christopher W. Ward ◽  
Espen E. Spangenburg ◽  
Reagan M. Nelson
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Force Production ◽  
Contractile Apparatus ◽  
Actomyosin Atpase ◽  
Functional Aspects ◽  
Intact Muscle ◽  
Cross Bridges ◽  
Muscle Contractile

This study examined the effects of fatigue on the functional aspects of the contractile apparatus and sarcoplasmic reticulum (SR). Frog semitendinosus muscles were stimulated to fatigue, and skinned fibers or a homogenate fraction was prepared from both fatigued and rested contralateral muscles. In fatigued fibers, maximal Ca2+-activated force of the contractile apparatus was unaltered, whereas maximal actomyosin-ATPase activity was depressed by 20%. The Ca2+ sensitivity of force was increased, whereas that of actomyosin-ATPase was not altered. Also, the rate constant for tension redevelopment was decreased at submaximal Ca2+ concentration. These latter findings suggest that fatigue slows the dissociation of force-generating myosin cross bridges. Ca2+ uptake and Ca2+-ATPase activity of the SR were depressed by 46 and 21%, respectively, in the fatigued muscles. Fatigue also reduced the rates of SR Ca2+ release evoked by AgNO3 and 4-chloro- m-cresol by 38 and 45%, respectively. During fatigue, the contractile apparatus and SR undergo intrinsic functional alterations. These changes likely result in altered force production and energy consumption by the intact muscle.

scholarly journals Glucose 6-phosphate alters rat skeletal muscle contractile apparatus and sarcoplasmic reticulum function

1998 ◽  
Vol 83 (4) ◽  
pp. 489-502 ◽  
Author(s):  
JH Williams ◽  
CW Ward ◽  
EE Spangenburg ◽  
R Nelson ◽  
S Stavrianeas ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Contractile Apparatus ◽  
Rat Skeletal Muscle ◽  
Muscle Contractile

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

2004 ◽  
Vol 82 (7) ◽  
pp. 438-447 ◽  
Author(s):  
Kanu R Shah ◽  
Pallab K Ganguly ◽  
Thomas Netticadan ◽  
Amarjit S Arneja ◽  
Naranjan S Dhalla
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Congestive Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Muscle Fatigue ◽  
Ace Inhibitors ◽  
Renin Angiotensin System ◽  
Exercise Intolerance ◽  
Angiotensin System

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 (AT1R) 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.Key words: skeletal muscle, sarcoplasmic reticulum, Ca2+-transport, SR Ca2+-pump, congestive heart failure, renin-angiotensin system.

Myocardial calcium cycling defect in furazolidone cardiomyopathy

1991 ◽  
Vol 69 (12) ◽  
pp. 1833-1840 ◽  
Author(s):  
Peter James O'Brien ◽  
Hua Shen ◽  
Janice E. Weiler ◽  
S. Mehdi Mirsalimi ◽  
Richard J. Julian
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Ruthenium Red ◽  
Channel Activity ◽  
Release Channel ◽  
Calcium Sequestration ◽  
Pump Activity ◽  
Highly Correlated ◽  
Sarcoplasmic Reticulum Calcium

We have previously demonstrated that in furazolidone-induced congestive heart failure in turkeys the specific Ca2+-ATPase activity of myocardial sarcoplasmic reticulum (SR) is 60% increased in compensation for a 50% depression in net Ca2+-sequestration activity. This study tested the hypothesis that SR Ca2+-uptake and Ca2+-ATPase activities were uncoupled in this cardiomyopathy because of increased Ca2+-release channel activity. A novel microassay was used to monitor Ca2+ transport by myocardial homogenates using the fluorescent Ca2+ dye indo 1 to indicate extravesicular ionized Ca2+. The method is applied to cyropreserved biopsy specimens of myocardium and requires only 50 mg tissue. Both SR Ca2+-pump and SR Ca2+-channel activity were estimated using the channel-inhibitor ruthenium red (RR) and the mitochondrial inhibitor sodium azide. The specificity of the RR inhibition was confirmed using ryanodine. Cardiomyopathy was induced in 2-week-old turkey pouits by the addition of 0.07% furazolidone to their feed for 4 weeks. Compared with controls, myocardial maximal Ca2+-channel activity relative to maximal Ca2+-pump activity was 22% greater and duration of Ca2+-channel activity was 100% increased. However, the heart failure birds had 43 and 53% decreases in absolute maximal Ca2+-pumping and Ca2+-channel activities, respectively. The abnormal Ca2+-channel activity resulted in 200% greater time before initiation of net Ca2+ sequestration and 700% greater final myocardial Ca2+ concentrations. For all birds, the Ca2+-accumulating activity was highly correlated with Ca2+-release activity (all p < 0.05). These data indicate that in this animal model of congestive heart failure there is defective SR Ca2+-channel function resulting in abnormal Ca2+ homeostasis. However, this defect can only partially explain our previous finding of furazolidone-induced uncoupling of Ca2+ uptake from Ca2+-ATPase activities. The consequent myocardial Ca2+ overload predisposes the heart to fatigue and irreversible failure.Key words: sarcoplasmic reticulum, calcium sequestration, furazolidone cardiomyopathy, indo 1 spectrofluorometry.

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