Increase in the (Na+ + K+)-ATPase activity in heart muscle after chronic treatment with digitoxin or potassium deficient diet

1976 ◽  
Vol 37 (1) ◽  
pp. 189-191 ◽  
Author(s):  
Viktor Bluschke ◽  
Rainer Bonn ◽  
Kurt Greeff
1977 ◽  
Vol 72 (2-3) ◽  
pp. 133-139 ◽  
Author(s):  
H. J. Reiermann ◽  
J. W. Herzig ◽  
J. C. Rüegg
Keyword(s):  

Biologia ◽  
2017 ◽  
Vol 72 (6) ◽  
Author(s):  
Nazanin Bohlooli Ghashghaee ◽  
King-Lun Li ◽  
Wen-Ji Dong

AbstractContractility of the heart muscle is a result of sliding movements between thick and thin filaments, produced by interactions between actin and myosin during the cross-bridge cycle. Activation of the myofilament is triggered by Ca


1970 ◽  
Vol 34 (1) ◽  
pp. 13-19 ◽  
Author(s):  
SEITOKU MIZUNO ◽  
SHIGERU TAKAMATSU ◽  
YUICHI TAMADA ◽  
KOHEI ARAYA ◽  
AKIHIKO TAKAHASHI ◽  
...  

1965 ◽  
Vol 209 (1) ◽  
pp. 8-16 ◽  
Author(s):  
Allan C. Stam ◽  
Carl R. Honig

The influence of adrenergic mediators on the Mg-stimulated actomyosin ATPase of glycerinated cardiac myofibrils was analyzed. The mediators increased ATPase activity in the presence of soluble cardiac relaxing substance, but were without effect in its absence. Mechanical changes in the fibrils accompanied changes in ATPase activity. Threshold concentrations were: dl-isoproterenol = 3 x 10–8 m, l-epinephrine = 7 x 10–8 m, and l-norepinephrine = 6 x 10–7 m. Dichloroisoproterenol and dichloroepinephrine decreased ATPase activity in both the presence and absence of relaxing substance. The depressant effects of the dichloro analogs were not altered by epinephrine and isoproterenol, and could account for adrenergic "blockade" in vivo. Evidence of the specificity of myofibrillar enzyme, relaxing substance, and adrenergic stimulus is presented. Comparison of the properties of the cardiac inotropic adrenergic receptor with the properties of the soluble cardiac relaxing system suggests that the latter constitutes an intracellular site of action of adrenergic mediators in heart muscle.


1979 ◽  
Vol 20 (5) ◽  
pp. 699-699
Author(s):  
Hideaki Higashino ◽  
Takao Yanagawa ◽  
Aritomo Suzuki

2014 ◽  
Vol 92 (1) ◽  
pp. 78-84 ◽  
Author(s):  
Athina A. Strilakou ◽  
Stylianos T. Tsakiris ◽  
Konstantinos G. Kalafatakis ◽  
Aikaterini T. Stylianaki ◽  
Petros L. Karkalousos ◽  
...  

Choline is an essential nutrient, and choline deficiency has been associated with cardiovascular morbidity. Choline is also the precursor of acetylcholine (cholinergic component of the heart’s autonomic nervous system), whose levels are regulated by acetylcholinesterase (AChE). Cardiac contraction–relaxation cycles depend on ion gradients established by pumps like the adenosine triphosphatases (ATPases) Na+/K+-ATPase and Mg2+-ATPase. This study aimed to investigate the impact of dietary choline deprivation on the activity of rat myocardial AChE (cholinergic marker), Na+/K+-ATPase, and Mg2+-ATPase, and the possible effects of carnitine supplementation (carnitine, structurally relevant to choline, is used as an adjunct in treating cardiac diseases). Adult male albino Wistar rats were distributed among 4 groups, and were fed a standard or choline-deficient diet for one month with or without carnitine in their drinking water (0.15% w/v). The enzyme activities were determined spectrophotometrically in the myocardium homogenate. Choline deficiency seems to affect the activity of the aforementioned parameters, but only the combination of choline deprivation and carnitine supplementation increased myocardial Na+/K+-ATPase activity along with a concomitant decrease in the activities of Mg2+-ATPase and AChE. The results suggest that carnitine, in the setting of choline deficiency, modulates cholinergic myocardial neurotransmission and the ATPase activity in favour of cardiac work efficiency.


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