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)

Adrenaline was infused intravenously in nine normal volunteers to plasma concentrations similar to those found after myocardial infarction. This study was undertaken on three occasions after 5 days' treatment with placebo or the beta-adrenoceptor antagonists, atenolol or timolol. Adrenaline increased the systolic pressure by 11 mmHg, decreased the diastolic pressure by 14 mmHg, and increased the heart rate by 7 beats/min. These changes were prevented by atenolol. However, after timolol the diastolic pressure rose (+19 mmHg) and heart rate fell (-8 beats/min). Adrenaline caused the corrected QT interval (QTc) to lengthen (0.36 +/- 0.02 s to 0.41 +/- 0.06 s). No significant changes were found in the QTc when subjects were pretreated with atenolol or timolol. The serum potassium fell from 4.06 to 3.22 mmol/l after adrenaline. Serum potassium fell to a lesser extent to 3.67 mmol/l after atenolol and actually increased to 4.25 mmol/l after timolol. Adrenaline-mediated hypokalaemia appears to result from the stimulation of a beta 2-adrenoceptor linked to membrane Na+/K+-ATPase causing potassium influx.
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PMID:The effects of cardioselective and non-selective beta-adrenoceptor blockade on the hypokalaemic and cardiovascular responses to adrenomedullary hormones in man. 686 46

Magnesium ions are important for maintaining the functional and structural integrity of the myocardium. Epidemiologic studies suggest that myocardial hypomagnecytia can predispose to sudden cardiac death and that hard water protective factor preventing heart attack could be magnesium. Recent studies show that infarcted portion of the myocardium has lowered magnesium content as compared to noninfarcted segment. Magnesium deficiency sensitises the myocardium to the toxic effect of various drugs, hypoxia etc. and magnesium administration is protective. The metabolic, biochemical and electrophysiologic effects of magnesium appear to be significant in treatment of myocardial ischaemia. Magnesium is a metal-coenzyme and activates adenosine-triphosphatase which may be inhibited by nonglucose fuels like lactate and free fatty acids. Magnesium deficiency may be responsible for the chronic electrical instability of the myocardium predisposing to sudden cardiac death. The acute precipitating stress dependent trigger which lie in the brain may also be related to magnesium. In addition to fast Na and Ca channels there could be a Mg-carrying transport system maintaining the electrical activity of the myocardium. There is sufficient evidence to suggest the use of magnesium salts against ischaemic heart disease and sudden cardiac death. Magnesium is cardioprotective and influences action potential duration, membrane potential and perhaps maintains the fast response. The therapeutic and prophylactic value of magnesium needs further assessment.
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PMID:Magnesium in atherosclerotic cardiovascular disease and sudden death. 697 57

In chronic heart failure, the inter-relationship of the renin-angiotensin-aldosterone system (RAAS) and cardiac growth is of primary clinical interest. In the pressure or volume overloaded heart, hypertrophic growth of the myocardium includes the enlargement of cardiac myocytes--an adaptation governed by ventricular loading. Nonmyocyte cell growth involving cardiac fibroblast may also occur but not primarily regulated by the hemodynamic load. Cardiac fibroblast activation is responsible for the accumulation of fibrillar type I and type III collagens within the interstitium and adventitia of intramyocardial coronary arteries. In addition to relaxation abnormalities due to impairment of sarcoplasmic Ca(2+)-ATPase activity, this remodeling of the cardiac interstitium represents a major determinant of pathological hypertrophy in that it accounts for abnormal myocardial stiffness, leading to ventricular diastolic and systolic dysfunction and ultimately the appearance of symptomatic heart failure. In vivo and in vitro studies suggest that the effector hormones, angiotensin II and aldosterone, of the RAAS are primarily involved in regulating the structural remodeling of the myocardial collagen matrix. In cultured adult cardiac fibroblasts, angiotensin II and aldosterone have been shown to stimulate collagen synthesis while angiotensin II additionally inhibits matrix metalloproteinase 1 activity, which is the key enzyme for interstitial collagen degradation in the myocardium. These observations may serve as rationale why angiotensin converting enzyme inhibition or blockade of the RAAS represents such remedial therapy in congestive heart failure in patients with hypertensive heart disease, post-myocardial infarction or with dilated cardiomyopathy.
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PMID:Myocardial collagen matrix remodeling and congestive heart failure. 763 1

The effects of dietary supplementation with eicosapentaenoic acid (EPA) on ventricular arrhythmias during myocardial infarction were examined in a canine model. EPA was incorporated into cellular membranes after ingestion of EPA-ester (100 mg/kg body weight/day) for 8 weeks. The ratio of EPA to arachidonic acid (AA) in platelet cell membranes and myocardial microsomes was significantly increased (7% to 37% in platelet cell membranes; p < 0.01, 3% to 12% in non-infarcted cardiac microsomes; p < 0.01, and from 2% to 8% in infarcted cardiac microsomes; p < 0.01). Dietary supplementation with EPA significantly reduced the incidence and severity of arrhythmias during coronary artery occlusion. Immediately after coronary artery occlusion, all of the animals in the control group that were given a toxic dose of digitalis developed ventricular tachycardia (VT) or ventricular fibrillation (Vf), whereas none of the animals in the EPA-supplement group developed VT or Vf within 15 min after administration of digitalis. Regardless of the presence of an infarcted area, the specific activity of the Ca(2+)-pump enzyme ((Ca(2+)-Mg2+)-ATPase) within the myocardial microsomal fraction of the EPA-supplemented group was significantly higher than in that of the control group (Vmax: 140.5 +/- 19.1 vs 94.8 +/- 28.9 nmol/mg/min in non-infarcted cardiac microsomes, p < 0.01, 130.9 +/- 18.4 vs 90.2 +/- 26.4 nmol/mg/min in infarcted cardiac microsomes, p < 0.01, EPA vs control group, respectively). The specific activities of the Na(+)-pump enzyme ((Na(+)-K+)-ATPase) and NADPH-dependent cytochrome C reductase in infarcted and non-infarcted cardiac microsomes did not differ between these groups. These results indicate that EPA supplementation increases the (Ca(2+)-Mg2+)-ATPase activity within myocardial membranes that is involved in Ca2+ metabolism in myocardial cells by increasing the ratio of EPA to AA within cellular membranes. These cellular alterations are likely to reduce the severity of ventricular arrhythmias by inhibiting the rapid accumulation of intracellular Ca2+ following ischemia.
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PMID:Antiarrhythmic effects of eicosapentaenoic acid during myocardial infarction--enhanced cardiac microsomal (Ca(2+)-Mg2+)-ATPase activity. 769 37

The systems regulating the levels of Ca(2+)-Mg2+, Ca(2+)-ATPase and potential-dependent absorption of Ca2+ as well as content of cyclic nucleotides, beta-adrenoreceptors, activities of adenylate-, guanylate cyclases and phosphodiesterase were studied in the synaptosomes of rat brain cortex in evolving myocardial infarction. In addition, reverse absorption of noradrenaline, dopamine and serotonin was studied. In one of the animal groups myocardial infarction was simulated after stress. The myocardial infarction, affecting the systems of Ca2+ regulation, caused an increase in reverse absorption of dopamine and serotonin simultaneously with accumulation of lactate in the synaptosomes. In myocardial infarction developed after stress adenylate cyclase was activated, reverse absorption of dopamine was decreased and the content of lactate tended to decrease as compared with the infarction formed without stress effects.
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PMID:[Systems for regulating the level of Ca2+, cyclic nucleotides, and reverse absorption of neurotransmitters in isolated nerve endings of the rat brain during development of myocardial infarct]. 809 86

The interrelationships of magnesium (Mg) and potassium (K) homeostasis are reviewed. Evidence from clinical and experimental studies including whole animal and cell culture experiments indicate that (1) homeostasis of Mg and K are closely related in the whole organism, (2) deficiencies of Mg and K frequently co-exist with gastrointestinal and especially renal losses from diuretic and nephrotoxic drug treatment being mainly responsible, and (3) Mg is required for maintenance of normal cellular K. Evidence from many laboratories indicate that Mg has direct effects at a cellular level on K transport. These include effects on Na-K-ATPase, Na-K-Cl cotransport, K channels, charge screening and permeability effects on membranes. New data on positive correlations between Mg and K in cardiac tissue, skeletal muscle and lymphocytes from patients undergoing cardiopulmonary bypass are presented. Interrelationships in Mg and K in cardiac tissue have probably the greatest clinical significance in terms of arrhythmias, digoxin toxicity, and myocardial infarction. Future studies will be aimed at elucidating mechanisms of Mg-K interrelationships at a cellular level using new techniques with the ability to detect concentrations and modulations of free intracellular Mg.
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PMID:Interrelationships of magnesium and potassium homeostasis. 826 16

Myocardial infarction in rats induced by occluding the left coronary artery for 4, 8 and 16 weeks has been shown to result in congestive heart failure (CHF) characterized by hypertrophy of the viable ventricular myocardial tissue. We have previously demonstrated a decreased calcium transport activity in the sarcoplasmic reticulum (SR) of post-myocardial infarction failing rat hearts. In this study we have measured the steady state levels of the cardiac SR Ca(2+)-pump ATPase (SERCA2) mRNA using Northern blot and slot blot analyses. The relative amounts of SERCA2 mRNA were decreased with respect to GAPDH mRNA and 28 S rRNA in experimental failing hearts at 4 and 8 weeks post myocardial infarction by about 20% whereas those at 16 weeks declined by about 35% of control values. The results obtained by Western blot analysis, revealed that the immunodetectable levels of SERCA2 protein in 8 and 16 weeks postinfarcted animals were decreased by about 20% and 30%, respectively. The left ventricular SR Ca(2+)-pump ATPase specific activity was depressed in the SR preparations of failing hearts as early as 4 weeks post myocardial infarction and declined by about 65% at 16 weeks compared to control. These results indicate that the depressed SR Ca(2+)-pump ATPase activity in CHF may partly be due to decreased steady state amounts of SERCA2 mRNA and SERCA2 protein in the failing myocardium.
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PMID:Decreased expression of cardiac sarcoplasmic reticulum Ca(2+)-pump ATPase in congestive heart failure due to myocardial infarction. 897 68

Abnormalities intrinsic to skeletal muscle are thought to contribute to decrements in exercise capacity found in individuals with chronic heart failure (CHF). Na+-K+-adenosinetriphosphatase (the Na+ pump) is essential for maintaining muscle excitability and contractility. Therefore, we investigated the possibility that the number and affinity of Na+ pumps in locomotor muscles of rats with CHF are decreased. Myocardial infarction (MI) was induced in 8 rats, and a sham operation was performed in 12 rats. The degree of CHF was assessed approximately 180 days after surgery. Soleus and plantaris muscles were harvested, and Na+ pumps were quantified by using a [3H]ouabain binding assay. At the time of muscle harvest, MI and sham-operated rats were similar in age (458 +/- 54 vs. 447 +/- 34 days old, respectively). Compared with their sham-operated counterparts, MI rats had a significant amount of heart failure, right ventricular-to-body weight ratio was greater (48%), and the presence of pulmonary congestion was suggested by an elevated lung-to-body weight ratio (29%). Left ventricular end-diastolic pressure was significantly increased in the MI rats (11 +/- 1 mmHg) compared with the sham-operated controls (1 +/- 1 mmHg). In addition, mean arterial blood pressure was lower in the MI rats compared with their control counterparts. [3H]ouabain binding sites were reduced 18% in soleus muscle (136 +/- 12 vs. 175 +/- 13 pmol/g wet wt, MI vs. sham, respectively) and 22% in plantaris muscle (119 +/- 12 vs. 147 +/- 8 pmol/g wet wt, MI vs. sham, respectively). The affinity of these [3H]ouabain binding sites was similar for the two groups. The relationship between the reduction in Na+ pump number and the reduced exercise capacity in individuals with CHF remains to be determined.
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PMID:Decreased [3H]ouabain binding sites in skeletal muscle of rats with chronic heart failure. 921 79

Rats are generally believed to be insensitive for cardiac glycosides. However, like in humans, the hemodynamic effects may be related to the pathophysiological condition. Since the hemodynamic effects of cardiac glycosides have never been investigated in rats with heart failure, the aim of the present experiments was to investigate the role of the pathophysiological condition in the rat. Therefore, hemodynamic and cardiac effects of ouabain were investigated both in normal rats and rats with heart failure due to myocardial infarction (MI). Since the effects of ouabain may also depend on the treatment scheme, rats were treated either for a short-term period or a long-term period. Three weeks after sham surgery or ligation of the left coronary artery (MI), Wistar rats were treated for two weeks with ouabain (14.4 mg/kg.d s.c.), either continuously (osmotic minipumps) or intermittently (once daily). A separate group of rats was treated for 45-60 min (1-100 microg/kg.min ouabain; i.v. infusion 5 weeks after MI). Hemodynamic measurements were performed at rest and after volume loading in conscious rats, chronically instrumented with an electromagnetic flow probe and catheters. Induction of MI resulted in a significant increase in total peripheral resistance (TPR), and a significant decrease in basal and maximal cardiac output following volume loading (basal CO: sham, 92 +/- 5; MI, 74 +/- 5 ml/min; maximal CO: sham, 152 +/- 4; MI, 105 +/- 7 ml/min; n = 7-11). Chronic intermittent ouabain treatment further increased TPR in MI rats. In contrast, continuous ouabain treatment normalized TPR in rats. Only in continuously treated MI rats, basal and maximal CO improved significantly (basal: 83 +/- 4; maximal: 134 +/- 7 ml/min; n = 7). Acute treatment dose-dependently worsened the hemodynamic conditions of MI rats, since TPR and MAP increased and CO and stroke volume decreased significantly. These experiments demonstrate that ouabain can improve cardiac function in rats, although only in MI rats and strongly depending on the delivery regimen. Thus, in contrast to the general belief, the presently used rat model is suitable for investigation of cardiac glycosides in heart failure. The preferential improvement of cardiac function in MI rats continuously treated with ouabain may depend upon changes in Na+,K+-ATPase or altered neurohumoral conditions due to MI and chronic treatment.
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PMID:Ouabain improves cardiac function in vivo in rats with heart failure after chronic but not acute treatment. 927 26

"Remodeling" implies changes that result in rearrangement of normally existing structures. This review focuses only on permanent modifications in relation to clinical dysfunction in cardiac remodeling (CR) secondary to myocardial infarction (MI) and/or arterial hypertension and includes a special section on the senescent heart, since CR is mainly a disease of the elderly. From a biological point of view, CR is determined by 1 ) the general process of adaptation which allows both the myocyte and the collagen network to adapt to new working conditions; 2) ventricular fibrosis, i.e., increased collagen concentration, which is multifactorial and caused by senescence, ischemia, various hormones, and/or inflammatory processes; 3) cell death, a parameter linked to fibrosis, which is usually due to necrosis and apoptosis and occurs in nearly all models of CR. The process of adaptation is associated with various changes in genetic expression, including a general activation that causes hypertrophy, isogenic shifts which result in the appearance of a slow isomyosin, and a new Na+-K+-ATPase with a low affinity for sodium, reactivation of genes encoding for atrial natriuretic factor and the renin-angiotensin system, and a diminished concentration of sarcoplasmic reticulum Ca2+-ATPase, beta-adrenergic receptors, and the potassium channel responsible for transient outward current. From a clinical point of view, fibrosis is for the moment a major marker for cardiac failure and a crucial determinant of myocardial heterogeneity, increasing diastolic stiffness, and the propensity for reentry arrhythmias. In addition, systolic dysfunction is facilitated by slowing of the calcium transient and the downregulation of the entire adrenergic system. Modifications of intracellular calcium movements are the main determinants of the triggered activity and automaticity that cause arrhythmias and alterations in relaxation.
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PMID:Molecular mechanisms of myocardial remodeling. 992 72


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