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 effects of carnosine on erythrocyte membrane Na,K-ATPase and isolated enzyme in vitro as well as on membrane Na,K-ATPase activity and lipid peroxidation (LPO) in chronic heart failure (CHF) and acute myocardial infarction (AMI) have been studied. CHF and AMI have been shown to be associated with significant inhibition of the erythrocyte membrane Na,K-ATPase activity and LPO activation. Marked activation of erythrocyte membrane Na,K-ATPase by carnosine in comparison with the isolated enzyme has been established. The ability of carnosine to induce Na,K-ATPase activation and prevent membrane depolarization indicates that the dipeptide may be a useful tool in the pathogenetic therapy of CFH and AMI.
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PMID:[The effect of carnosine on the activity of Na,K,ATPase: prospective uses in clinical cardiology]. 133 6

We studied alterations in respiratory activity of mitochondria (Mt) in non-infarcted myocardium (NIZ) under severe pump failure complicated by acute myocardial infarction (AMI). Dogs in which AMI was induced were divided into two groups; one in which left ventricular systolic pressure (LVPs) was maintained higher than 70% of preligation level (ND group); and one in which LVPs was diminished to less than 70% (D group). Regional myocardial blood flow (MBF) in NIZ reduced significantly in proportion to decreases in LVPs and cardiac output (CO). State -III activity and RCR decreased in proportion to reductions in MBF, LVPs, and CO in Mt from NIZ of D group. Complex-I and DNP-stimulated ATPase activities were also reduced in NIZ of D group. Morphologic studies revealed slight swelling and fusion of mitochondria in NIZ cells of D group, but no changes such as the appearance of a dense deposit indicating ischemic damage were seen. Pump failure in AMI is likely to be caused partly by impaired function of Mt in NIZ induced by hypoperfusion. Improvement of metabolic impairment in NIZ is important in the treatment of pump failure.
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PMID:Impairment of mitochondrial respiratory activity of non-infarcted myocardium under severe pump failure in acute myocardial infarction. 183 71

Epinephrine was infused intravenously in 9 normal volunteers to plasma concentrations similar to those found after acute myocardial infarction. This study was undertaken on 3 occasions after 5 days of treatment with placebo or the beta-adrenoceptor antagonist, atenolol, which is relatively beta 1 selective, or timolol, which blocks both beta 1 and beta 2 receptors. Epinephrine increased the systolic blood pressure (BP), decreased the diastolic BP and increased the heart rate modestly. These changes were prevented by atenolol. However, after timolol the diastolic BP rose by +19 mm Hg and heart rate fell by -8 beats/min. Epinephrine caused the corrected QT interval to lengthen (0.36 +/- 0.02 to 0.41 +/- 0.06 second). No significant changes were found in the corrected QT interval when subjects were pretreated with atenolol or timolol. The serum potassium decreased from 4.06 to 3.22 mmol/liter after epinephrine. Serum potassium decreased to a lesser extent to 3.67 mmol/liter after atenolol and actually increased to 4.25 mmol/liter after timolol. In a further study with a similar design another nonselective beta blocker propranolol also increased potassium after epinephrine. While atenolol also prevented hypokalemia in this study, it did not block the beta 2-receptor mediated decrease in diastolic BP. Epinephrine-induced hypokalemia results from stimulation of a beta-adrenoceptor linked to membrane sodium/potassium adenosine triphosphatase causing potassium influx. This appears to be predominantly mediated by beta 2 receptors although beta 1 receptors may also play a part.
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PMID:Epinephrine-induced hypokalemia: the role of beta adrenoceptors. 301 Jun 93

The effects of different beta-adrenoceptor agonists and antagonists on plasma noradrenaline and potassium concentrations were studied in patients with borderline hypertension. Heart rate, arterial pressure and the heart rate corrected duration of total electromechanical systole (QS2I) were also measured. Infusion of the beta-adrenoceptor agonists isoprenaline (non-selective) and salbutamol (beta 2-selective), but not prenalterol (beta 1-selective) caused dose-dependent increments in plasma noradrenaline. Isoprenaline and salbutamol decreased plasma potassium dose-dependently. For a given effect on heart rate and QS2I the fall in potassium was less pronounced after prenalterol. The effects of isoprenaline were also studied after the beta-adrenoceptor antagonists propranolol, 320 mg day-1 for 1 week (non-selective) and atenolol, 100 mg day-1 for 1 week (beta1-selective). The effects of isoprenaline, when infused in equipotent chronotropic doses, on noradrenaline and potassium were not affected by atenolol, whereas they were completely abolished by propranolol. The rise in noradrenaline during beta-adrenoceptor stimulation could be explained by presynaptic facilitation of noradrenaline release. The fall in potassium probably reflects stimulation of Na-K-ATPase dependent transport of potassium into the cell. Both effects were seen after beta 2- but not after beta 1-adrenoceptor stimulation. Hypokalaemia and raised levels of noradrenaline are also known to occur under such stressful conditions as acute myocardial infarction, when circulating levels of the endogenous beta 2-adrenoceptor agonist adrenaline are high. Blockade of these effects by beta-adrenoceptor antagonists may contribute to the cardioprotective effect of these drugs. This warrants further consideration of the clinical significance of beta-blocker selectivity.
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PMID:Cardioprotection by blockade of beta 2-adrenoceptors. 613 69

Coronary heart diseases (CHD) have high indices of mortality and morbidity. A number of CHD and myocardial ischaemic syndromes such as unstable angina pectoris, sudden death ischaemic heart disease, acute myocardial infarction and ventricular arrhythmias have been associated with losses of myocardial magnesium and potassium. Mg++ ions are essential for regulation of Na+ and K+ transport across cell membranes, including those found in cardiac and vascular smooth muscle cells. Mg++ activates an Na+-K+-ATPase pump which in turn plays a major role in regulating Na+-K+ transport. Loss of cellular Mg++ results in loss of critically important phosphagens: MgATP and creatine phosphate. Thus, under conditions where cellular Mg++ is depleted (e.g. hypoxia, ischaemia, anoxia), the Na+-K+ pump and phosphagen stores will be compromised, leading to alterations in resting membrane potentials. Cellular Mg++ depletion has been found to result in concomitant depletion of K+ in a number of cells, including cardiac and vascular muscles. The consequences of these events are often production of cardiac arrhythmias. Myocardial and vascular injury lead to disturbances in electrolyte transport across cell membranes, whereby Na+ and Ca++ uptakes are enhanced and, just prior or concomitantly, Mg++ and K+ are lost. Such electrolyte disturbances often lead to necrotic foci. Considerable evidence has accumulated to indicate that the extracellular concentration of Mg++ is important in control of arterial tone and blood pressure via pressure via regulation of vascular membrane Mg++-Ca++ exchange sites. A reduction in the extracellular Mg++ concentration can produce hypertension, coronary vasospasm and potentiation of vasoconstrictor agents by allowing excess entry of Ca++; concomitantly, the potency of vasodilator agents is reduced. Alterations in vascular membrane Mg++ results in arterial and arteriolar membranes which are 'leaky', thus contributing to the cellular reduction in K+ and gain of Na+ and Ca+. Alterations in extracellular K+ or Na+ concentrations over physiological ranges, in the face of a Mg++ deficit, can exacerbate the coronary vasospasm noted with reduction in only extracellular Mg++. Since free Mg++ ions are necessary for maintaining Ca+ ions (both plasma membrane-bound and sarcoplasmic reticulum membrane-bound via Ca++ ATPases), intracellular free Mg++ would rise in conditions which result in cellular loss of Mg++, thereby exacerbating and contributing to elevation of blood pressure and coronary vasospasm.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Magnesium, electrolyte transport and coronary vascular tone. 614 22

Metabolic effects of dexamethasone (DX) on the noninfarcted functioning myocardium were studied in rabbits with experimental coronary artery ligation to evaluate the usefulness of glucocorticoids in acute myocardial infarction. Maximum active tension of noninfarcted area of the isolated perfused hearts was markedly reduced 6 hr, 2 days, and 5 days after ligation, associated with significant decreases in norepinephrine (NE) and cAMP contents, but with no changes in adenylate cyclase (AC) and cAMP phosphodiesterase (PDE) activities. Calcium content of mitochondrial fraction was considerably increased in the peri- and noninfarcted area without any changes in microsomal CA2+ or myocardial total Ca2+. Ca2+ uptake rate and Ca2+-dependent ATPase activity of the sarcoplasmic reticulum fraction from the operated hearts were markedly reduced. Intramuscular administration of DX (3 mg/kg body wt/day) for 2 days after operation significantly improved these reductions in myocardial function and metabolism. In normal hearts from animals without infarction, DX caused 48% elevation in basal cAMP level, marked reductions in mitochondria and microsomal Ca2+, and 26% decrease in PDE activity, although no changes in myocardial total Ca2+ AC activity and myocardial contractility were observed. NE-induced inotropic effects were markedly enhanced in both control and operated groups with DX treatment. These results indicated that large doses of DX would improve the reduced myocardial function and metabolism in acute myocardial infarction by increasing basal cAMP level and by its influence on intracellular Ca2+ available for cellular activity.
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PMID:The effects of large doses of dexamethasone on myocardial contractility and calcium metabolism in experimental myocardial infarction. 742 58

Magnesium (Mg), a cofactor in numerous enzymatic reactions, is often ignored by clinicians, as the symptomatology of Mg depletion is not specific and usually associated with that of the cause of the depletion. Furthermore, the plasma Mg concentration (0.8 to 1.1 mmol.L-1) is only equivalent to one percent of the total body content. A Mg deficit may exist while plasma Mg concentration is normal. Therefore other techniques for Mg assessment, such as the repletion test, as well as red blood cell and lymphocyte concentrations have been used. A renewed interest for Mg occurred as numerous studies have shown the therapeutic efficiency of Mg and as the mechanisms of its haemodynamic effects have been recognized. Mg regulates Na-K-ATPase activity, K channels activity and, most of all, it is a natural calcium channel blocking agent. These properties explain its important place in electrophysiology of myocardial cells and the effects on the tension of smooth muscles, resulting in a vasodilation and a bronchodilation respectively. The antagonistic effect of Mg on calcium decreases the presynaptic release of acetylcholine at the neuromuscular junction and the release of epinephrine at the peripheral sympathetic nerves and the adrenals. Mg potentiates the effect of non-depolarizing muscle relaxants. A Mg deficiency occurs often in ICU patients, in alcoholics and during use of diuretics. Simultaneous administration of Mg is often required for treatment of potassium deficiency. Mg has an anti-arrhythmic effect towards digoxin-mediated dysrhythmias and torsades de pointes, and can be efficient in other arrhythmias. Systematic use of Mg seems to decrease mortality of acute myocardial infarction and is justified during cardiac surgery, often associated with hypomagnesemia, because of vasodilation of coronary arteries and in order to prevent occurrence of arrhythmias. Mg, because of its calcium channel blocking properties and as it lowers the release of epinephrine, is indicated for surgery of pheochromocytoma. In eclamptic and pre-eclamptic patients, the use of Mg is valuable, but not as an anti-epileptic agent. Other clinical uses of Mg have been proposed, but they are either anecdotal or of uncertain efficiency.
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PMID:[Indications for the use of magnesium in anesthesia and intensive care]. 857 7

Recent evidence suggests the existence of several endogenous Na+,K+-ATPase inhibitors in mammals. Previously, we have shown that the amphibian Na+,K+-ATPase inhibitor marinobufagenin (3,5-dihydroxy-14,15-epoxy bufodienolide) acts as a vasoconstrictor in isolated rat and human arteries. Mammalian plasma was shown to contain marinobufagenin-like immunoreactive material, which is responsive to saline volume expansion. The present study describes purification of a bufodienolide, which is similar to marinobufagenin, from the urine of patients after acute myocardial infarction with the use of thin-layer chromatography and reverse-phase high-performance liquid chromatography (HPLC). The purified substance cross-reacted with marinobufagenin antibody, demonstrated maximal UV absorbance at 300 nm characteristic of bufodienolides, and eluted from HPLC columns with the same retention time as marinobufagenin. Mass spectrometry of purified material revealed the presence of a substance indistinguishable from amphibian marinobufagenin and having molecular mass of 400 D. The present studies show that one of the human digitalis-like factors may have a bufodienolide structure and is likely to represent marinobufagenin or its isomer, and they suggest a role for this substance in the pathogenesis of myocardial ischemia.
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PMID:Characterization of a urinary bufodienolide Na+,K+-ATPase inhibitor in patients after acute myocardial infarction. 957 20

One of the reasons of ventricular arrhythmias and coronary artery spasms in patients with acute myocardial infarction (AMI) may be the lower Na(+)-K(+)-ATPase activity, which causes decrease of potassium intracellular concentration and increase of calcium intracellular concentration. The aim of the study was the examination of the rate of sodium efflux through the lymphocytic cell membrane in patients with AMI after thrombolytic therapy. The survey was made in 50 patients with AMI after thrombolytic therapy: 30 of them with reperfusion (group I) and 20 without reperfusion (group II). The control group consisted of 31 healthy persons. Rates of total, ouabain-sensitive and furosemide-sensitive sodium efflux through the lymphocytic cell membrane were measured before thrombolysis, then 3 and 5 days after, using the method elaborated by Haegerty et al. All patients were treated with aspirin, glyceryl trinitrate and thrombolysis therapy with alteplase (r-TPA). In all patients with AMI rates of total and ouabaine-sensitive sodium efflux through the lymphocytic cell membrane were decreased, but rates of furosemide-sensitive sodium efflux were normal. In patients after thrombolytic therapy with reperfusion, 3 and 5 days after thrombolysis the decreased rates were normal, but they were still decreased in patients without reperfusion.
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PMID:[Sodium efflux through lymphocytic cell membranes in patients with acute myocardial infarction]. 1040 67

In a rat model of acute myocardial infarction (MI) produced by coronary artery ligation, thyroid hormone metabolism was altered with significant reductions (54%) in serum triiodo-L-thyronine (T(3)), the cellular active hormone metabolite. T(3) has profound effects on the heart; therefore, rats were treated with T(3) after acute MI for 2 or 3 wk, at either replacement or elevated doses, to determine whether cardiac function and gene expression could be normalized. Acute MI resulted in a 50% (P < 0.001) decrease in percent ejection fraction (%EF) with a 32-35% increase (P < 0.01) in compensatory left ventricle (LV) hypertrophy. Treatment of the MI animals with either replacement or elevated doses of T(3) significantly increased %EF to 64 and 73% of control, respectively. Expression levels of several T(3)-responsive genes were altered in the hypertrophied LV after MI, including significant decreases in alpha-myosin heavy chain (MHC), sarcoplasmic reticulum calcium-activated ATPase (SERCA2), and Kv1.5 mRNA, whereas beta-MHC and phospholamban (PLB) mRNA were significantly increased. Normalization of serum T(3) did not restore expression of all T(3)-regulated genes, indicating altered T(3) responsiveness in the postinfarcted myocardium. Although beta-MHC and Kv1.5 mRNA content was returned to control levels, alpha-MHC and SERCA2 were unresponsive to T(3) at replacement doses, and only at higher doses of T(3) was alpha-MHC mRNA returned to control values. The present study showed that acute MI in the rat was associated with a fall in serum T(3) levels, LV dysfunction, and altered expression of T(3)-responsive genes and that T(3) treatment significantly improved cardiac function, with normalization of some, but not all, of the changes in gene expression.
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PMID:Thyroid hormone metabolism and cardiac gene expression after acute myocardial infarction in the rat. 1109 20


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