Muscle adenosine triphosphatase

Contraction of muscle follows an increase of Ca " in the muscle cell as a result of nerve stimulation. This initiates processes which cause the proteins myosin and actin to be drawn together making the cell shorter and thicker. The return of the Ca " to its storage site, the sarcoplasmic reticulum, by an active pump mechanism allows the contracted muscle to relax (27). Calcium ion, also a factor in the release of acetylcholine on stimulation of nerve cells, influences the permeabiUty of cell membranes activates enzymes, such as adenosine triphosphatase (ATPase), Hpase, and some proteolytic enzymes and facihtates intestinal absorption of vitamin B 2 [68-19-9] (28). 

Voluntary muscles contain a variety of fibre types which are specialized for particular tasks. Most muscles contain a mixture of fibre types although one type may predominate. All human skeletal muscles are composed of several different muscle fibre types. Up to seven different fibre types have been identified histochemically based on the pH stability of myofibrillar adenosine triphosphatase and on the myosin heavy chain profile. Innumerable fibre type transients exist due to continuing adaptation processes. However, three main... 

The catecholamines can play an important role in the short-term regulation of plasma potassium levels. Stimulation of hepatic a-adrenoceptors will result in the release of potassium from the liver. In contrast, stimulation of (32-adrenoceptors, particularly in skeletal muscle, will lead to the uptake of potassium into this tissue. The (32-adrenoceptors are linked to the enzyme Na"", K+ adenosine triphosphatase (ATPase). Excessive stimulation of these (32-adrenoceptors may produce hypokalemia, which in turn can be a cause of cardiac arrhythmias. 

In vitro studies of gingerol using canine cardiac tissue and rabbit skeletal muscle demonstrated Ca2+-adenosine triphosphatase (ATPase) activation in the cardiac and skeletal sarcoplasmic reticulum (SR) (31). Gingerol (3-30... 

P5. Pennington, R. J., Biochemistry of dystrophic muscle mitochondrial succinate-tetrazolium reductase and adenosine triphosphatase. Biochem. J. 80, 649-654 (1961). 

Sreter, F. A., Seidel, J. C., and Gergely, J., Studies on myosin from red and white skeletal muscles of the rabbit. I. Adenosine triphosphatase activity. J. Biol. Chem. 241, 5772-5776 (1966). 

Caldesmon is a cytoplasmic protein with two isoform classes, one of which is found predominantly in smooth muscle cells and other cell types with partial myogenic differentiation. High-molecular-weight isoforms with molecular weights between 89 and 93 kD are capable of binding to actin, tropomyosin, calmodulin, myosin, and phospholipids, and they function to counteract actin-tropomyosin-activated myosin adenosine triphosphatase (ATPase). As such, they are mediators for the inhibition of calcium-dependent smooth muscle contraction." ... 

Sokolova, V. E., Effect of ascorbic acid on the activity of adenosine triphosphatase of heart and skeletal muscle of the guinea pig. Biochemistry (U.S.S.R.) (English translation) 21, 475-478 (1956). 

At relevant inotropic and vasorelaxant concentrations, milrinone is a selective inhibitor of peak III cAMP phosphodiesterase isozyme in cardiac and vascular muscle. This inhibitory action is consistent with cAMP-mediated increases in intracellular ionized calcium and contractile protein phosphorylation and relaxation in vascular muscle. Additional experimental evidence also indicates that milrinone is not a beta-adrenergic agonist nor does it inhibit sodium-potassium adenosine triphosphatase activity as do the digitalis glycosides. 

The magnitudes of entropies of activation have provided valuable information regarding the details of the interactions between enzymes and substrates. The process of muscular contraction involves an interaction between the muscle enzyme myosin and adenosine triphosphate (ATP). Myosin is an enzyme which catalyzes the hydrolysis of ATP, a process which we have seen (p. 246) to be more exergonic than is the case for many other phosphates, and this hydrolysis contributes energy for contraction. Because of its catalytic action, myosin is also referred to as adenosine triphosphatase (ATP-ase). When the activated complex is formed from ATP ase and its substrate ATP, the entropy of activation is about 41 cal K" mol under approximately normal physiological conditions. We saw on p. 400, on the basis of a very simple electrostatic theory of AS values for ionic reactions in aqueous solution, that there will be a positive contribution of about 10 cal mol for each unit of the product [ [ % ( The long myosin molecules bear a series of positive... 

The mechanism whereby cardiac glycosides cause a positive inotropic effect and electrophysiological changes is still not completely known despite years of active investigation. Several mechanisms have been proposed, but the most widely accepted mechanism involves the ability of cardiac glycosides to inhibit the membrane-bound Na /K -adenosine triphosphatase (Na /K -ATPase) pump responsible for sodium/potassium exchange. To understand better the correlation between the pump and the mechanism of action of cardiac glycosides on the heart muscle contraction, one has to consider the sequence of events associated with cardiac action potential that ultimately leads to muscular contraction. The process of membrane depolarization/repolarization is controlled mainly by the movement of the three ions, Na", K", Ca ", in and out of the cell. 

Another possibility deserving consideration is that some of the phytoestrogen effects may be attributable to properties that do not involve estrogen receptors, such as effects on enzymes, protein synthesis, cell proliferation, angiogenesis, calcium transport, Na /K adenosine triphosphatase, growth factor action, vascular smooth muscle cells, lipid oxidation, and cell differentiation. Some of these properties will be further discussed. 

In the aorta of normal rabbits fed on stock diet, lactic dehydrogenase, NADH-tetrazolium reductase and adenosine triphosphatase are active in smooth-muscle fibres between elastic lamellae (Adams et al. 1963). Within 4 weeks on a cholesterol-enriched diet, macrophages infiltrate or proliferate in the thickened intima of the aorta and these cells react strongly with the lactic dehydrogenase, NADH-tetrazolium reductase and adenosine triphosphatase methods. 

The circulating and intracellular calcium participate in many vital metabolic reactions muscle contraction, neuromuscular excitability, blood coagulation, adenosine triphosphatase activations, and other reactions. 

The activity of ion transport systems, such as sodium- and potassium-activated adenosine triphosphatase, has been studied In vivo by the use of rubidium-87 MRS. This has been possible because rubidium has been shown to substitute for potassium in a number of transmembrane transport systems, accumulating in the intracellular space. Standard in vitro methods of determining Na+/K+-ATPase activity, which also use rubidium, give highly variable measurements and in some cases contradictory results. Many of these problems appear to have been overcome by the use of in vivo Rb MRS, especially when sequential measurements are required. In a longitudinal study of spontaneously hypertensive rats, Rb MRS showed that skeletal muscle rubidium rose at a faster rate in hypertensive rats than in control animals, which is consistent with a marked increase in Na+/K+-ATPase activity. This type of experiment emphasizes the value of in vivo MRS since rubidium kinetics can be determined sequentially on the same animal, minimizing inter/intra-subject variability as well as the number of animals required in the study. 

A low intake of magnesium may also contribute to a higher mortality of cardiovascular disease in soft water areas. Magnesium -and also calcium - are involved in enzyme systems in the heart muscle. Sealig (1972) (54) has shown for example that inadequate magnesium concentration interferes with the activation of adenosin-triphosphatase and causes a loss of potassium by myocardial cells. This might be responsible for sudden death from coronary artery disease. 

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