Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present paper shows the arrhythmogenic effect of a direct induction of lipid peroxidation (LP) on isolated auricles; it is demonstrated that preendured stress potentiates this effect, while antioxidants prevent it. Subsequently, in studying the mechanism of the LP arrhythmogenic effect it was established that stress, like the LP induction, disorders the activity of Na, K-ATPase and accelerates thermodenaturation of this enzyme which plays a key role in maintaining the transmembrane potential and the electrical stability of the heart. Antioxidants prevent the enumerated shifts. Based on these data, the antioxidant BHT was successfully applied for prevention of the fall in cardiac fibrillation threshold in stress and experimental myocardial infarction, and also for prevention of cardiac fibrillation itself under acute ischemia and reoxygenation of the heart.
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PMID:The role of lipid peroxidation in pathogenesis of arrhythmias and prevention of cardiac fibrillation with antioxidants. 303 69

We investigated the effectiveness of the beta-blocking agent metipranolol in preventing detrimental systemic and myocardial alterations induced in healthy dogs by adrenaline (AD) infused at a rate which mimics spontaneous secretion after coronary occlusion. Metipranolol (0.3 mg/kg) was infused intravenously concurrently with AD (1.2 micrograms/kg/min) for 4 h and blood values of free fatty acids (FFA) and triiodothyronine(T3) were measured initially, after 2 and 4 h of infusion and compared with those obtained in dogs infused with AD alone and with saline. Metipranolol suppressed a rise in free fatty acid, reversed AD-induced histoenzymatic changes in succinic dehydrogenase and ATPase activity and considerably inhibited the development of mitochondrial alterations detected in dogs infused with AD alone. A tendency to attenuate AD-induced fall in serum T3 was also detected in metipranolol-treated dogs. Results suggest that this drug might be of value in preventing consequences of increased adrenergic activity in the acute stage of myocardial infarction.
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PMID:Prevention of adrenaline-induced metabolic systemic and myocardial alterations by the beta-blocking agent metipranolol in the dog. 611 91

Human postmortem cardiac muscle was studied by immunofluorescent microscopy. Necrotic cells in acute myocardial infarctions were first identified with the hematoxylin-eosin stain as showing hypereosinophilia and autofluorescence. The results of the immunofluorescence staining showed a marked decrease if not absence of labeling for the Ca+ and Mg+ adenosine triphosphatase (ATPase) and tropomyosin in all necrotic muscle cells within a myocardial infarction. Myocytolytic cells located at the border of the infarct showed a labeling intensity similar to that of normal muscle cells. The use of immunofluorescence localization of muscle-specific proteins can be used as a reliable method to detect myocardial cell necrosis.
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PMID:Immunofluorescent microscopy for the identification of human necrotic myocardium. 614 3

Ultracytochemical changes in ATPase activity of ischemic myocardial cells were studied in the dog heart by electron microscopy in the early stage of myocardial infarction and compared to the fine structural alterations in the ischemic myocardium. 1) In the normal myocardial cell, ATPase activity was observed intensely in the terminal cisternae (TC) of the sarcoplasmic reticulum (SR), and moderately in the myofilaments in the longitudinal SR and around the gap junctions of the intercalated discs. 2) The most striking change in the ischemic myocardial cells was the reduction in the ATPase reaction product in the TC of the SR and along the gap junctions 60 min after coronary ligation, simultaneously with swelling of the TC and the appearance of mitochondrial dense deposits. The reaction product began to decrease at 30 min on the myofilaments, and for 3 to 12 hours no reaction product was observed except irreversible morphologic changes in 60 to 70% of the longitudinal SR in the ischemic subendocardial cells. 3) A decrease in ATPase activity was recognized in the early stage of myocardial ischemia simultaneously with the fine structural changes of myocardial cells and it is considered to be one of the signs of ischemic irreversibility.
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PMID:Electron microscopic studies on the ATPase activity in myocardial infarction -changes in the early myocardial infarction. 621 2

Experiments on rabbits with experimental myocardial infarction were made to determine the content of adenyl nucleotides and Ca2+-dependent ATPase activity of myosin outside the zone of necrosis. It was found that on the 5th day the animals injected with 40 mg/kg riboxine intravenously on a daily basis manifested a 36% increase in the content of AMP and a 81% increase in the CA2+-dependent ATPase activity as compared with untreated controls. Injection of riboxine did not produce any appreciable changes in the content of ATP and ADP. Riboxine appears to stimulate the utilization of the energy of macroenergic binding of adenyl nucleotides with myocardial cells.
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PMID:[Effect of riboxine on the ATPase activity and adenine nucleotide content in the myocardium in experimental myocardial infarct]. 622 79

Acute heart ischemia induced by ligation of the left coronary artery is associated with variation in the activity of acetylcholinesterase, Na, K-ATPase and Ca, Mg-ATPase in rat erythrocytes. The maximum pronounced variations in the enzymatic activity and in the membrane capacity of erythroblasts for binding direct turquoise are recorded on the 7th day of the experimental myocardial infarction.
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PMID:[Changes in acetylcholinesterase and ATPase activity and certain structural features of the erythrocyte membrane in experimental myocardial ischemia]. 625 88

Changes in the cardiac sarcolemma in myocardial infarction were studied by both determination of Na+-K+-ATPase activity and SDS gel electrophoretic analysis of sarcolemmal proteins in the canine heart. Ninety minutes after coronary ligation, Na+-K+-ATPase activity in ischemic myocardium was decreased significantly to approximately 36% of that of non-ischemic myocardium, and it remained at the lower level for 28 days. By SDS gel electrophoresis, reduction of the protein band with molecular weight of 111,000, which is suggestive of the main component of ATPase, was observed simultaneously with the reduction of Na+-K+-ATPase activity. These results indicate that ischemia for 90 minutes produces substructural changes in the sarcolemma indicating irreversible myocardial changes.
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PMID:Studies on the Na+-K+-ATPase in myocardial infarction. 627 94

Specific binding sites have been demonstrated to exist in the heart for several drugs and hormones such as beta-blocking agents, cardiac glycosides, catecholamines, insulin, glucagon and acetylcholine. The specific binding sites for cardiac glycosides in the human heart have certain properties which make it likely that they are the pharmacological receptors for the therapeutic and toxic actions of digitalis glycosides: they are located in the cell membrane and bind cardioactive steroids reversibly with high affinity: half-maximal receptor binding occurs at approximately 2 nM (approximately 1.5 ng/ml) for digoxin; potassium decreases receptor affinity, calcium increases it; specific binding of ouabain, digoxin or digitoxin is related to inhibition of (Na+ + K+)-ATPase activity--which is supposed to be the receptor enzyme for cardiac glycosides. Human left ventricle contains approximately 1.5 x 10(14) binding sites/g wet weight, right ventricle approximately 0.9 x 10(14). In disease the number of receptors may decrease (hypothyroid states, myocardial infarction) or increase (hyperthyroidism, chronic hypokalaemia). Certain drugs (such as phenytoin) or different temperatures or pH changes cause a change in digitalis-receptor affinity. Thus, the number of receptors and possibly their properties are subject to regulation in clinically relevant situations. Further investigations will probably reveal those pathophysiological states, which allow the explanation of toxicity or digitalis refractoriness.
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PMID:The cardiac glycoside-receptor system in the human heart. 630 38

1. Alterations in troponin subunits in myocardial infarction were studied in the dog heart by the analysis of troponin-tropomyosin complex, i.e, native tropomyoin, of total structural proteins in SDS gel electrophoresis, and by the measurement of degree of activation of actomyosin-ATPase by Ca++. 2. At 12 to 24 hours after coronary ligation, reductions in TN-C and tropomyosin were observed followed by a decrease in TN-I at 48 hours. The relative contents of these subunits were the lowest at 72 hours to 7 days falling to less than 10% of those in the non-ischemic myocardium. On the contrary, TN-T was preserved through the course of myocardial infarction. 3. Actomyosin-ATPase activity was increased at 12 to 24 hours after coronary ligation and then reduced rapidly at 24 to 48 hours together with the degradation of myosin. However, the activation of actomyosin-ATPase by Ca++-troponin-tropomyosin was reduced already at 12 hours simultaneously with the reduction in TN-C, and almost completely lost at 48 hours. 4. Troponin subunits and actomyosin-ATPase activity returned to those of the control myocardium at 28 days after coronary ligation indicating the recovery of infarcted tissue.
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PMID:Alterations in cardiac troponin subunits in myocardial infarction. 645 21

The interactions of Mg and K in cardiovascular disease are diverse and complex. However, Mg deficiency and loss from the heart and arteries, caused e.g. by dietary deficiency or imbalance, or by diseases and their treatment, can contribute to cardiovascular damage, and to functional abnormalities. Although Mg deficiency interferes with K retention, it is seldom measured in routine clinical practice, and the need to correct low Mg levels, in order to replete K, is rarely considered. The heart, with its high metabolic activity, is particularly vulnerable to Mg deficiency or loss because of the importance of Mg in mitochondrial structure and enzymatic function. The need for Mg to activate Na/K ATPase has long been known. Mg has also been shown to be structurally part of the enzyme in cardiac mitochondria. Additionally, Na/K exchange occurs in association with phosphorylation and dephosphorylation, reactions that are also Mg-dependent. The demonstration that Mg modulates K+/proton (H+) exchange, and that cation selectivity in Na+ and K+ exchange for H+ is highly dependent on the concentration of Mg++, provides new insights into how Mg protects against K loss. The loss of myocardial K that results from Mg deficiency contributes to electrophysiologic changes, as can the Ca shifts of Mg loss. A high Ca/Mg ratio also predisposes to arterial spasms, and increases catecholamine release. Thus the arrhythmogenic potential of Mg deficiency can be related to imbalances between Mg and K or between Mg and Ca, or both. Electrical or K-induced catecholamine release is increased by a low Mg/Ca ratio, as are increased fatty acids and lipids and intravascular hypercoagulability. K or Ca loading of the patient with undiagnosed Mg inadequacy is not only often unsuccessful, but it may carry inherent risks. It can intensify the Mg depletion, the arterial contractility, and ECG abnormality. In the patient receiving digitalis, Mg deficiency can increase drug toxicity. In the case of myocardial infarction, Mg deficiency can increase the risk of malignant ventricular arrhythmias and sudden cardiac death. In the absence of alcoholism or gastrointestinal disease, the use of loop diuretic therapy for congestive heart failure, especially in elderly patients, is the most common cause of Mg depletion. A high concurrence of hypomagnesemia with hypokalemia, from whatever cause, has been documented. However, systemic Mg deficiency can exist despite normal Mg serum levels. Methodological difficulties hamper direct detection of cellular Mg deficiency, but patients can be indirectly evaluated by use of Mg-loading tests, which may be of combined diagnostic and therapeutic value.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions of magnesium and potassium in the pathogenesis of cardiovascular disease. 653 39


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