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 clinical syndrome of heart failure occurs as a consequence of the limitation of compensatory mechanisms, such as cardiac hypertrophy. To clarify transcriptional changes in specific genes in failing hearts, we examined the expression of cardiac Ca(2+)+Mg(2+)-dependent ATPase in the sarcoplasmic reticulum and transforming growth factor beta genes in the ventricles of rat hypertrophied heart, and the expression of guanine nucleotide-binding protein and "fetal" contractile protein genes in the ventricles of cardiomyopathic Syrian hamsters of Bio14.6. Northern blot analysis of total cellular RNA revealed that the mRNA levels of Ca(2+)+Mg(2+)-dependent ATPase were decreased by pressure overload and became 32% of sham in 1 month, and were correlated with corresponding protein levels. Transforming growth factor beta mRNA, a potent activator of collagen synthesis, was increased by pressure overload. The expression levels of the Gs alpha mRNA, which stimulated the adenylate cyclase, in Bio14.6 ventricles were lower than the levels in ventricles of the F1B hamster strain, and decreased as the stage of cardiomyopathy progressed. Moreover, re-expression of fetal mRNA was observed in the ventricle of cardiomyopathic Syrian hamsters of the Bio14.6 strain. These results indicate that reprogramming of cardiac gene expression both of myofibrillar and nonmyofibrillar components might occur in the failing heart.
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PMID:Molecular mechanism of hypertrophied failing heart--abnormalities of the diastolic properties and contractility. 138 37

This report compares the effects of adrenalectomy and thyroidectomy, with and without hormone replacement, on loss of contractile protein ATPase activities. The rationale for this study was derived from the similarities in their intracellular receptors, mechanisms of action, and the large number of proteins regulated by both hormones. Rats were adrenalectomized, thyroidectomized, or both, and were subsequently treated for 6 weeks with hydrocortisone, triiodothyronine, or saline. Sham-operated rats were given saline for the same period of time. Six weeks of adrenal insufficiency resulted in diminished enzymatic activity of myofibrillar, Ca(2+)-activated myosin ATPase, and actin-activated myosin ATPase fractions. Treatment with hydrocortisone prevented the decline in enzymatic activity due to adrenalectomy. Likewise, thyroidectomy caused a loss of enzymatic activity which was prevented by treatment with triiodothyronine. The full deleterious effect of combined ablation could be partially prevented by treatment with either hydrocortisone or triiodothyronine, but the latter was most effective. The results suggest that hydrocortisone and triiodothyronine each had significant positive effects in the presence of the other, but not in its absence, on the activity of myofibrillar Ca(2+)-dependent Mg-ATPase and Ca(2+)-activated myosin ATPase. The effects of these two hormones on actin-activated myosin ATPase activity were more independent of each other. We conclude that the actions of thyroid and glucocorticoid hormones on the heart are interrelated and that optimum myocardial function results from their combined action.
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PMID:Myocardial contractile protein ATPase activities in adrenalectomized and thyroidectomized rats. 148 85

Cardiac adaptation to hemodynamic stress involves both quantitative (hypertrophy) and qualitative (pattern of gene expression) changes. Our previous studies have shown that advancing age in the rat is associated with diminished capacity to develop left ventricular hypertrophy in response to either ascending aortic constriction (AoC). In this study, we examined whether the expression of protooncogenes and contractile protein genes in response to AoC differs between adult (9-mo-old) and old (18-mo-old) rats. RNA was isolated from the left ventricles of AoC animals of both age groups subjected to a similar hemodynamic stress. Immediately after AoC, the levels of the ventricular expression of c-fos and c-jun protooncogenes were markedly lower in the old rats than in the adult animals. 5 d after the operation, the ratio of beta- to alpha-myosin heavy chain mRNAs increased significantly after AoC in both age groups. In contrast, AoC was associated with a marked reduction in the levels of mRNAs encoding sarcoplasmic reticulum Ca(2+)-ATPase (by 69%) and cardiac calsequestrin (by 49%) in the old rats but not in the adults. The mRNAs encoding atrial natriuretic factor and skeletal alpha-actin increased in response to AoC only in the adult rats. There were no significant differences in expression of the cardiac alpha-actin mRNA among the experimental groups. These data suggest that (a) the expression of protooncogenes in response to acute pressure overload is significantly reduced in the aged rats and (b) the pattern of expression of the contractile protein gene in response to AoC in the old rats differs qualitatively as well as quantitatively from that in younger animals. These age-related differences may play a role in the higher frequency of heart failure in the aged during hemodynamic stress.
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PMID:Age-related differences in the expression of proto-oncogene and contractile protein genes in response to pressure overload in the rat myocardium. 153 37

To determine the effects of chronic nonocclusive coronary constriction on cardiac hemodynamics, myocardial structure, and contractile protein enzyme activity, the left coronary artery was narrowed in rats, and measurements of ventricular pump function, extent and localization of tissue damage, and myofibrillar Mg2+ and Ca2+ myosin adenosinetriphosphatase (ATPase) activities were measured 3 mo later. In the presence of coronary artery stenosis averaging 56%, two different degrees of depression in global cardiac performance were identified, and the animals were divided in two groups. In the first group, left ventricular end-diastolic pressure (LVEDP) was increased and LV+ and/or--the first derivative of LV pressure (dP/dt) were decreased, whereas in the second group end-diastolic and peak systolic LV pressures, LV+ and -dP/dt and right ventricular dynamics were all impaired. Thus left ventricular dysfunction and failure occurred with coronary narrowing. Structurally, multiple foci of replacement fibrosis were found across the left ventricular wall, but the number of these lesion profiles was 2.6-fold larger in failing animals than in rats with cardiac dysfunction. Biochemically, Mg(2+)-ATPase activity in myofibrils and Ca2+ myosin ATPase were not altered biventricularly. On the other hand, a shift from V1 to V3 myosin isoenzymic content occurred in the failing left ventricle. In conclusion, the late impairment in ventricular pump function associated with prolonged coronary artery stenosis appears to be sustained more by the magnitude of myocardial damage than by defects in contractile protein enzyme activity.
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PMID:Long-term coronary stenosis in rats: cardiac performance, myocardial morphology, and contractile protein enzyme activity. 163 51

Changes in the contractile and fatigue properties of the cat diaphragm muscle were examined during the first 6 wk of postnatal development. Both twitch contraction time and half-relaxation time decreased progressively with age. Correspondingly, the force-frequency curve was shifted to the left early in development compared with adults. The ratio of peak twitch force to maximum tetanic force decreased with age. Fatigue resistance of the diaphragm was highest at birth and then progressively decreased with age. At birth, most diaphragm muscle fibers stained darkly for myofibrillar adenosinetriphosphatase after alkaline preincubation and thus would be classified histochemically as type II. During subsequent postnatal development, the proportion of type I fibers (lightly stained for adenosinetriphosphatase) increased while the number of type II fibers declined. At birth, type I fibers were larger than type II fibers. The size of both fiber types increased with age, but the increase in cross-sectional area was greater for type II fibers. On the basis of fiber type proportions and mean cross-sectional areas, type I fibers contributed 15% of total muscle mass at birth and 25% in adults. Thus postnatal changes in diaphragm contractile and fatigue properties cannot be attributed to changes in the relative contribution of histochemically classified type I and II fibers. However, the possibility that these developmental changes in diaphragm contractile and fatigue properties correlated with the varying contractile protein composition of muscle fibers was discussed.
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PMID:Diaphragm muscle fatigue resistance during postnatal development. 183 23

The effect of tellurite on ATPase activity of the contractile membrane protein in human erythrocytes was studied. Tellurite, even at a concentration of 0.01 mM, inhibited 25 per cent of the saponin-stimulated ATPase activity of the contractile membrane protein; the inhibition increased with increasing tellurite concentration, and was reversible. On the other hand, in erythrocytes preincubated with tellurite, the ATPase activity of the membrane contractile protein, non-stimulated by saponin, increased, and the increase was further enhanced by washing the erythrocytes. The behaviour is analogous to the tellurite effect on erythrocyte morphology: incubation of erythrocytes with tellurite caused morphological changes which were more pronounced after removing the tellurite by washing. The complex effect of tellurite is discussed.
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PMID:Tellurite effect on ATPase activity of contractile membrane protein. 183 76

Myosin of heart muscle shows ATPase activity. In the atrial myocardium, normal isozymic pattern was alpha dominant which converted to being beta dominant in an overloaded hypertrophy. In order to clarify the distribution of myosin isozymes in human heart, ATPase activity of the atrial myosin recovered from the patient underwent open heart surgery was determined. In the present study, ATPase activity of right atrial myosin from the heart with tricuspid regurgitation (TR) (group A (n = 6); 398.1 +/- 67.0 nmol pi/mg/min) was significantly less than that from the heart without TR (group B (N = 7); 533.9 +/- 62.4, p less than 0.05). The myosin ATPase activity showed correlation with systemic RA pressure (y = 0.019x + 19.6, r = -0.68429), systemic RV pressure (y = 0.039x + 58.67, r = 0.73484), SVI (y = 0.05x + 18.1, r = 0.87587) and RV maxDp/Dt (y = 0.42x + 589.9, r = -0.67493) (p less than 0.05). These data suggests that preoperative cardiac function involves in cardiomuscular structure with redistribution of contractile protein.
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PMID:[Secondary tricuspid insufficiency and right atrial myosin ATPase activity]. 214 12

The chronic treatment of spontaneously hypertensive rats (SHR) with 7,8-dimethyl-10-(3-chlorobenzyl) isoalloxazine [CBI], 7,8-diethyl-10-aminol isoalloxazine [DEAI], enduron (methyclothiazide) and amiloride were studied for their effects on blood pressure and cardiac contractile protein ATPase activities. After 35 weeks of treatment all the above antihypertensive agents showed a decrease in blood pressure in the SHR (p less than 0.01). Chronic treatment with CBI, DEAI, enduron, and amiloride significantly improved the myofibrillar ATPase activity at all pCa2+ concentrations (p less than 0.01). Furthermore, CBI, DEAI, enduron, and amiloride drug treatments enhanced actin-activated myosin ATPase activity (p less than 0.01). The Ca2(+)-activated myosin ATPase activity was significantly elevated after treating with CBI and DEAI (p less than 0.01). These results suggest that the antihypertensive agents used in this study helped in reducing the blood pressure with a subsequent increase in myocardial contractile protein ATPase activity.
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PMID:Effects of riboflavin analogues and diuretics on the spontaneously hypertensive rat heart. 214 69

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

Time-dependent alterations in integrated cardiovascular function were assessed in the streptozotocin-diabetic rat. Hemodynamic measurements in the intact, anesthetized animal revealed significant and progressive reduction in heart rate after 2, 4, and 8 weeks of diabetes. Myocardial contractility (+ dP/dt) and rate of relaxation (-dP/dt) were preserved at 2 weeks, but progressively declined thereafter. Integrative mechanisms maintained mean arterial blood pressure within normal limits at all time points. Pressure was regulated by minimizing cardiac output reduction via slight increases in stroke volume (Starling mechanism) and concomitant small increases in total peripheral resistance. In response to graded isoproterenol infusion and brief, total aortic occlusion, percent increase of heart rate and + dP/dt was maintained despite decrements in absolute values. Reduced peripheral vasodilation resulted in elevated sensitivity of the heart rate-blood pressure relationship during isoproterenol challenge. The -dP/dt was uniformly impaired in diabetic rats during isoproterenol infusion. When given a rapid saline infusion, diabetic hearts appropriately augmented volume output via the Starling mechanism. Initial hemodynamic abnormalities observed in the intact, diabetic rat are consistent with known defects in cardiac adrenergic receptor density, contractile protein ATPase activity, and sarcoplasmic reticulum calcium uptake. However, many cellular and subcellular defects are compensated by integrative hemodynamic mechanisms while latent alterations are observed only in the intact cardiovascular system.
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PMID:Integrative nature and time course of cardiovascular alterations in the diabetic rat. 242 82


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