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:3.6.4.1 (myosin ATPase)
1,140 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Daily administration of d,l isoproterenol-HCl (5 mg/kg) in rats for periods of 14-21 days results in marked cardiac hypertrophy and a decrease in cardiac actomyosin ATPase activity. Actomyosin suspensions (ionic strength 0.08) from right and left ventricles showed average decreases in ATPase activity of 37.1% (p less than 0.005) and 35.7% (p less than 0.05), respectively, for animals treated with isoproterenol for 14 days. Isolated myofibrils from combined ventricular muscle of another group of animals that received the same isoproterenol treatment showed an average decrease in ATPase of 36.4% (p less than 0.0025). The later experiments also demonstrated that the decrease in ATPase activity was not Ca++ sensitive suggesting the lack of involvement of a change in the calcium regulatory factors (tropomyosin-troponin complex). In contrast to these findings, purified myosin from treated animals and actomyosin assayed under conditions which essentially reflect myosin ATPase activity uninfluenced by actin interaction (actomyosin in solution, ionic strength 0.6), did not demonstrate a change in ATPase from controls. It was concluded that the decrease in cardiac actomyosin ATPase in isoproterenol treated rats involved primarily a defect in actin or the interaction of actin with other components of the contractile protein complex.
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PMID:Characterization of the decreased ATPase activity of rat cardiac actomyosin in isoproterenol-induced cardiac hypertrophy. 15 67

1. Experiments were carried out to examine the biochemical changes, such as contractile protein biochemistry and membrane bound enzyme alterations associated with skeletal muscles of myd/myd. 2. Our studies demonstrate that there was a progressive decline in myofibrillar ATPase activity, and this decrease is greatest in 30 weeks old animals of myd/myd as compared to controls. 3. The proteolytic activity of myofibrils isolated from myd/myd was significantly higher than controls. 4. There was no significant difference in Ca2+ ATPase activity of myosin and actin-activated myosin ATPase activity of myd/myd and their controls. 5. Mg2+ ATPase and Na(+)+K(+)-ATPase of myodystrophic SL showed significant increase compared to controls. 6. Isoproterenol stimulated adenylate cyclase activity was significantly lower in the SL of dystrophic mice compared to controls. 7. GTP+isoproterenol stimulate adenylate cyclase was significantly higher in control SL and SR when compared to SL and SR isolated from myd/myd. 8. Guanylate cyclase activity was greater in myodystrophic mice both in the absence and presence of Triton X-100. cGMP and cAMP phosphodiesterase activities were greater in dystrophic mice as compared to controls. 9. These observations suggest that there are significant changes in myofibrillar ATPase, myofibrillar protease and membrane bound enzymes of myd/myd compared to control.
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PMID:Myofibrillar and membrane-bound enzymes in skeletal muscle from myodystrophic mice. 135 51

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

To determine the effects of chronic nonocclusive coronary constriction on cardiac hemodynamics, structural integrity, and contractile protein enzyme activity, the left coronary artery was narrowed in rats, and measurements of ventricular performance, magnitude, and distribution of tissue damage and myofibrillar Mg2+ and Ca2+ myosin ATPase activities were evaluated 1 month later. In the presence of coronary artery stenosis averaging 58%, three levels of involvement of global cardiac performance were identified, and the rats were divided accordingly. In the first group, only left ventricular end-diastolic pressure (LVEDP) was increased; in the second group, LVEDP and left ventricular +dP/dt and/or -dP/dt were affected; and in the third group, LVEDP, left ventricular +dP/dt and -dP/dt, and right ventricular end-diastolic pressure were impaired. Thus, left ventricular moderate dysfunction, severe dysfunction, and failure occurred with coronary narrowing. On a structural basis, coronary constriction resulted in an ongoing process characterized by acute myocytolytic necrosis and foci of replacement fibrosis in different stages of healing. The number of these lesion profiles in the left ventricular myocardium increased 4.7-, 4.4-, and 8.3-fold in rats with moderate dysfunction, severe dysfunction, and failure, respectively. Biochemically, Mg(2+)-ATPase activity of myofibrils increased biventricularly when moderate dysfunction was present. However, this parameter decreased with the appearance of severe dysfunction, reaching control values in ventricular failure. Ca2+ myosin ATPase activity was reduced in the left ventricle of rats with severe dysfunction and failure, whereas it was elevated in the right ventricle of rats with severe dysfunction. In conclusion, a fixed lesion of the left main coronary artery with a modest reduction in vessel luminal diameter generates a conditioned state of the heart characterized by a continuous loss of myocytes and replacement scarring, which, in combination with alterations in contractile protein enzyme activity, may be responsible for a number of abnormalities in cardiac dynamics ranging from moderate dysfunction to pump failure.
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PMID:Chronic nonocclusive coronary artery constriction impairs ventricular function, myocardial structure, and cardiac contractile protein enzyme activity in rats. 153 Jul 79

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

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

Studies were conducted to examine the effects of chronic adrenalectomy (Adx) and adrenalectomy plus glucocorticoid replacement therapy on rat cardiac contractile protein ATPase activities. The Ca2+-dependent Mg-ATPase activity of myofibrils isolated from rat ventricles 3 weeks postadrenalectomy (Adx) was significantly decreased at all pCa2+ concentrations (P less than 0.01), compared to sham-operated (SO) rats. Similarly, Ca2+-, K+-EDTA, and actin-activated myosin ATPase activities of Adx rat hearts were markedly decreased below that of SO rats (P less than 0.01). Dexamethasone administration to Adx rats prevented the decrease of Ca2+- and K+-ATPase activities of myosin, but not of myofibrillar Ca2+-dependent Mg-ATPase or actin-activated myosin Mg-ATPase activities. These studies suggest that glucocorticoid insufficiency induced by adrenalectomy results in altered myocardial contractile protein ATPase activity which may underlie impaired cardiac performance.
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PMID:Changes in myocardial contractile protein ATPases in chronically adrenalectomized rats with and without glucocorticoid replacement. 252 74

The pathogenesis of reduced systolic left ventricular function in dilated cardiomyopathy is yet unclear. To analyze a possible involvement of contractile protein, function and structure of left ventricular myofibrils were examined in hearts of patients with advanced cardiomyopathy undergoing heart transplantation and in normal control hearts (from renal transplant donors). Myosin and actin content of the left ventricular myocardium was slightly reduced in cardiomyopathic hearts. Myofibrillar polypeptide composition was determined using two-dimensional electrophoresis and immunoblotting. No differences in constituting polypeptides were apparent, including Z-line proteins and proteins of the endosarcomeric lattice. M-line-bound creatine kinase was identical in both groups. Further, basal and maximal myofibrillar adenosine triphosphatase (ATPase) activities were unaltered in dilated cardiomyopathy. The structure of purified myosin was identical in both groups by the following criteria: electrophoretic mobility of native myosin, identical pattern of light chains after isoelectric focusing, identical cleavage peptides of myosin's heavy chain, and identical patterns after immunoblotting of heavy chain cleavage peptides using polyclonal antibodies generated against myosin from normal and cardiomyopathic ventricles. Ca2+-activated, K+-EDTA-activated and actin-activated myosin ATPase activities were identical in control and cardiomyopathic hearts. A structural alteration or functional defect of myofibrils does not seem to be primarily involved in the pathogenesis of reduced myocardial contractility in dilated cardiomyopathy.
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PMID:Structure and function of contractile proteins in human dilated cardiomyopathy. 258 58


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