Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.4.1 (myosin ATPase)
 1,140 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in cardiac metabolism in myocardial failure and after alcohol ingestion are discussed. The main effect of alcohol ingestion is loss of cardiac contractility. Since heart muscle does not contain alcohol dehydrogenase, its toxicity is probably the result of a direct toxic effect of ethanol and acetaldehyde on the myocardial cell, possibly involving various membrane systems. Alcohol inhibits mitochondrial respiration and the activity of enzymes in the tricarboxylic acid cycle, and its interferes with both mitochondrial calcium uptake and binding. Ethanol profoundly affects myocardial lipid metabolism. Acetaldehyde diminishes myocardial protein synthesis and inhibits Ca++-activated myofibrillar ATPase. In myocardial failure, a series of possibilities may be responsible for the loss of contractility. Excitation-contraction coupling could be disturbed at the level of the sarcolemma, at the sarcoplasmic reticulum, at the mitochondria, and between calcium and the regulatory proteins. Deficiencies in Ca++ delivery systems of excitation-contraction coupling on the myosin ATPase activity could be responsible for the dimunition in cardiac contractility. Mitochondrial function may also be involved, since mitochondria from failing human hearts are defective with respect to respiratory control and calcium accumulation. Under certain conditions, the relationship of mitochondria to calcium sequestration is very important in influencing contractility. The involvement of contractile and regulatory proteins in myocardial failure cannot be excluded.
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PMID:Cardiac metabolsim: its contributions to alcoholic heart disease and myocardial failure. 15 68

Ethanol consumption is known to affect cardiac and skeletal muscle. In vivo experiments on cardiac muscle showed that ethanol affects cardiac contractility and Vmax, suggesting that contractile proteins of the myocardium were affected by ethanol. Therefore, experiments were carried out to examine the effects of ethanol on the cardiac contractile protein ATPase activities. Cardiac myofibrils isolated from ethanol-fed hamsters showed a significant decrease in myofibrillar ATPase activities between pCa 6 and 4. On the other hand, addition of ethanol (0.1%) in vitro to cardiac myofibrils from control hamster had no significant effect on the ATPase activities, suggesting that hamsters need to be exposed for longer periods of time to induce demonstratable changes in the contractile protein ATPase activity. Actin-activated myosin ATPase activities were significantly lower in myofibrils from ethanol-fed hamsters at 1:1 and 1:2 ratios of myosin to actin. These investigations revealed that chronic (4 weeks) exposure of hamsters to ethanol reduced cardiac contractile protein ATPase activity, which may help explain impaired cardiac function in chronic alcoholics.
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PMID:Effects of acute and chronic ethanol on cardiac contractile protein ATPase activity of Syrian hamsters. 214 42