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)

A study of the sarcolemmal Na+K+ATPase in the left failing heart due to induced mitral insufficiency was made in dogs. The sarcolemmal Na+K+ATPase markedly increased in the failing left ventricle. There was no change in the ATPase in the nonfailing right ventricle of the same dog. It was observed that during the early period of mitral incompetence, when there was an increase in the index of myocardial contractility, there was also a decrease in the sarcolemmal Na+K+-ATPase activity. There was no change in the MPG++-ATPase of the sarcolemmal fractions of either the failing or nonfailing ventricle. These results indicate that sarcolemmal Na+K+-ATPase appears to be involved in the reduction of the myocardial contractility during heart failure.
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PMID:Myocardial sarcolemmal ATPase in dogs with induced mitral insufficiency. 13 98

A study of the alterations in the intracellular electrolytes in the left failing heart due to induced mitral insufficiency was made in dogs. The extracellular space increased significantly. There was no significant change in the plasma Na+ and Ca++. However, there was a significant decrease in the plasma K+. The ratio of wet weight to dry weight increased during mitral insufficiency, although not significantly. There were no significant changes in the tissue Na+, K+ and Ca++. However, there were significant decreases in the intracellular Na+ and Ca++, and tendency for an increase in the intracellular K+ during mitral insufficiency. These results suggest that the decrease in the myocardial contractility in chronic heart failure due to mitral insufficiency might be due to a decrease in the intracellular Ca++ and associated changes in Na+ and K+ as a result of increased sarcolemmal ATPase.
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PMID:Cardiac intracellular and blood electrolytes in chronic mitral insufficiency. 74 36

Force development and shortening by cardiac muscle occur as a result of the interaction between actin and myosin within the myofibrillar lattice. This interaction is dependent upon intracellular ionized calcium and is controlled by the troponin-tropomyosin regulatory proteins situated along the actin filament. In this study, we compared the myofibrillar content and myofibrillar Mg-ATPase activity of normal human ventricular muscle with that of ventricular muscle from patients in end-stage failure caused by coronary artery disease or cardiomyopathy and ventricular muscle from patients with heart failure due to mitral valve insufficiency. The results show that the amount of myofibrillar protein (mg/g wet wt ventricle) in hearts in end-stage failure (coronary artery disease and cardiomyopathy) is significantly lower compared with normal hearts and hearts in failure due to mitral valve insufficiency. However, the Mg-ATPase activity of myofibrils from hearts in both end-stage failure and failure due to mitral valve insufficiency is significantly lower compared with myofibrils from normal hearts. The data suggest that the reduction in the amount of myofibrillar protein in ventricular tissue is a pivotal event that may be responsible for the progression of heart disease to the point of end-stage failure.
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PMID:Changes in myofibrillar content and Mg-ATPase activity in ventricular tissues from patients with heart failure caused by coronary artery disease, cardiomyopathy, or mitral valve insufficiency. 296 7

Prazosin has been used in the treatment of congestive heart failure. It is, however, not known whether prazosin gives only haemodynamic benefit or if it also produces a decrease in the cardiac sarcolemmal Na+-K+-ATPase which has been reported to be increased in the failing heart. The present investigation deals with the effect of 3 months of prazosin treatment in dogs with 3 months of induced mitral insufficiency (MI) on the sarcolemmal Na+-K+-ATPase activity. The dogs were divided into four groups each comprising of five dogs. A--normal; B--3 months of MI; C--6 months of MI; D--3 months of prazosin treatment after 3 months of MI. Three months of MI produced a decrease in the dp/dt and an increase in the end-diastolic pressure of left ventricle but no change in the index of left ventricular contractility and cardiac index. Also there was no change in the sarcolemmal Na+-K+-ATPase. There was a significant decrease in the index of left ventricular contractility and cardiac index and an increase in the LVEDP associated with a significant increase in the left ventricular sarcolemmal Na+-K+-ATPase at 6 months of MI. Sarcolemmal Mg2+-ATPase of both ventricles increased after 6 months of MI the significance of which is not known as yet. There was no change in the sarcolemmal Na+-K+-ATPase of the nonfailing right ventricle. Prazosin treatment prevented the deterioration of the left ventricular contractility and function and also prevented the increase in the sarcolemmal Na+-K+-ATPase observed in failing heart.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prazosin treatment on the cardiac sarcolemmal ATPase in failing heart due to mitral insufficiency in dogs. 299 Jul 14

This study was designed to determine whether digoxin therapy in the canine heart failing because of mitral regurgitation (MR) provides only hemodynamic benefit and accompanying subjective improvement or if it also reverses the changes in intracellular Ca++ and sarcolemmal Na+-K+-ATPase. The dogs were divided into four groups: control, MR of 3 months' duration, MR of 6 months', and digoxin treatment for 3 months after 3 months of MR. Six months of MR produced a marked decrease in the index of myocardial contractility and function associated with a decrease in intracellular Ca++ and Na+, and an increase in intracellular K+, extracellular space, sarcolemmal Na+-K+-ATPase, and Mg++-ATPase. Digoxin treatment tended to return the changes in the index of myocardial contractility and cardiac function, intracellular Ca++, Na+, K+, extracellular space, and sarcolemmal Na+-K+-ATPase of the failing heart toward control levels. Digoxin treatment did not affect Mg++-ATPase. The right ventricle, which did not fail, also did not show any significant changes in the parameters measured. The results showed that digoxin treatment not only improved the index of myocardial contractility and cardiac function of the failing heart but also tended to return the electrolytes and sarcolemmal Na+-K+-ATPase toward control levels.
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PMID:Effects of chronic digoxin treatment on cardiac function, electrolytes, and sarcolemmal ATPase in the canine failing heart due to chronic mitral regurgitation. 609 32

Myofibrillar but not actomyosin ATPase is depressed in failing myocardium from patients with dilated cardiomyopathy. Since there is a similar depression of myofibrillar ATPase in mitral regurgitation myocardium, we investigated whether or not the hydrolytic and mechanical performances of myosin are altered by comparing the maximal actomyosin ATPase activity and the in vitro myosin motility of myocardial myosin from patients with mitral regurgitation heart failure with that of patients with normal ventricular function. The results show that there is no significant difference (P > .05) between nonfailing and failing values for either the maximal actomyosin ATPase activity (0.3 s-1.head-1) or the myosin motility (1 micron/s). These observations suggest that changes, other than in the myosin heavy chain, contribute to the altered myocardial performance in mitral regurgitation myocardium.
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PMID:Maximal actomyosin ATPase activity and in vitro myosin motility are unaltered in human mitral regurgitation heart failure. 875 98

The aim of the study was to assess the impact of mitral regurgitation (MR) on left ventricular (LV) anatomic and molecular remodeling and function and to determine whether early LV remodeling and function predict long-term outcome in experimental organic MR. A new rodent model of chronic MR was created. Twenty-eight rats had surgically induced MR, twelve rats had a sham operation, and twelve rats had no operation. LV diameters, volume, and mass and LV ejection fraction (LVEF) and LV fractional shortening (LVFS) were assessed using echocardiography in the early stage of MR (6 and 12 wk after induction of MR). LV hemodynamics was assessed invasively. Cardiac alpha- and beta-myosin heavy chains and sarco(endo)plasmic reticulum Ca(2+)-ATPase 2 (SERCA2) were measured to assess molecular remodeling and contractility. Cox's proportional hazard ratios (HR) were used to identify outcome predictors. Early LV dilation was demonstrated in rats with MR when LVEF and LVFS were still normal. LV remodeling was associated with an increase in LV end-diastolic pressure and decrease in maximal change in pressure over time. Shifting of alpha- to beta-myosin and reduced SERCA2 were observed in rats with MR. Cox's proportional hazard analysis showed that LV end-diastolic diameters (HR, 1.2-2.4; P = 0.007) and LV end-diastolic volume (HR, 1.1-1.4; P = 0.005) at 6 wk and LV mass index (HR, 1.1-2.0; P = 0.004) at 12 wk after induction of MR were significantly associated with 1-yr mortality. However, LVEF (HR, 0.7-6.8 for the 6 wk, P > 0.05; and HR, 0.4-3.2 for the 12 wk, P > 0.05) and LVFS (HR, 0.4-1.4 for the 6 wk; and 0.4-3.1 for the 12 wk, P > 0.05) did not predict late death. Chronic MR leads to LV anatomic and cellular remodeling and impaired contractility. The time course of LV remodeling and function changes in the rat model of MR is similar to humans. Prediction of outcome may be achieved by assessments of early LV remodeling.
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PMID:Impact of mitral regurgitation on left ventricular anatomic and molecular remodeling and systolic function: implication for outcome. 1932 66

Congestive heart failure (HF) is associated with impaired endothelium-dependent nitric oxide-mediated vasodilatation. The aim of this study was to examine the effects of sarco/endoplasmic reticulum (ER) Ca(2+)-ATPase 2a (SERCA2a) gene transfer on endothelial function in a swine HF model. Two months after the creation of mitral regurgitation to induce HF, the animals underwent intracoronary injection of adeno-associated virus (AAV) carrying SERCA2a (n = 7) or saline (n = 6). At 4 months, coronary flow (CF) was measured in the mid-portion of the left anterior descending (LAD) artery. In the failing animals, CF was decreased significantly; SERCA2a gene transfer rescued CF to levels observed in sham-group [ml/min/g, 0.47 +/- 0.064 saline versus 0.89 +/- 0.116, SERCA2a; P < 0.05; 1.00 +/- 0. 185 sham P = NS (nonsignificant)]. In coronary arteries from HF animals, SERCA2a and endothelial isoform of nitric oxide synthase (eNOS) protein expression were decreased, but restored to normal levels by SERCA2a gene transfer. In human coronary artery endothelial cells (HCAECs), SERCA2a overexpression increased eNOS expression, phosphorylation, eNOS promoter activity, Ca(2+) storage capacity, and enhanced histamine-induced calcium oscillations, eNOS activity, and cyclic guanosine monophosphate (cGMP) production. Thus, SERCA2a gene transfer increases eNOS expression and activity by modulating calcium homeostasis to improve CF. These findings suggest that SERCA2a gene transfer improves vascular reactivity in the setting of HF.
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PMID:SERCA2a gene transfer enhances eNOS expression and activity in endothelial cells. 2046 Oct 63