Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:009336 (ATPase)
 59,826 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously shown that acute coronary occlusion in the dog is often accompanied by increased adrenaline release into the blood. In the present study the consequences of this humoral reaction were studied in anaesthetised healthy mongrel dogs subjected to adrenaline infusion administered at a rate relevant to spontaneous release of this amine in coronary occlusion. Adrenaline was infused in a dose of 1.2 microgram.kg-1.min-1 for 4 h. Dogs receiving saline served as the control. Adrenaline administration led to the decrease in insulin/glucose ratio, to a significant fall in serum triiodothyronine and in blood pH. Free fatty acid levels doubled. Histochemically, a diminution in succinic dehydrogenase and ATPase activity in adrenaline-treated hearts was found. A significant fall in the activity of mitochondrial hexokinase in these hearts was detected spectrophotometrically. Electron microscopic study revealed alterations in the mitochondrial structure. These findings indicate that an excess of adrenaline in ammounts similar to that seen in experimental infarction leads to profound metabolic and hormonal disturbances and exerts a detrimental effect upon myocardium.
Cardiovasc Res 1978 Mar
PMID:Evidence for the detrimental effect of adrenaline infused to healthy dogs in doses imitating spontaneous secretion after coronary occlusion. 2 14

The effects of glucagon in concentrations of 0.294 times 10(-6) mol/l, 1.47 times 10(-6) mol/l; 2.94 times 10(-6) mol/l, 5.8 times 10(-6) mol/l, and 1.47 times 10(-5) mol/l on the simultaneously recorded action potentials and contractions; and microsomal and sarcolemmal Na+-tk+-atpase in the myocardium of the guinea pig, rabbit, dog, and pig were investigated. Glucagon in all the concentrations produced an inhibition of the Na+-K+-ATPase associated with an increase in the contractility and shortening of the duration of action potential in dog myocardium. The increase in contraction was concentration-dependent up to a certain concentration. Inhibition of sarcolemmal ATPase was more than that of microsomal ATPase. In none of the concentrations did glucagon produce any significant changes in the Na+-K+-ATPase. In none of the concentrations did glucagon produce any significant changes in the Na+-K+-ATPase, contractility, and action potential duration in the myocardium of guinea pig, rabbit, or pig. These results suggest that glucagon-induced positive inotropic effect might be due to an increase in the Ca++ influx as a result of inhibition of membrane Na+-K+-ATPase. Shortening of the action potential duration might also be due to an increased efflux of potassium as a result of an inhibition of Na+-K+-ATPase.
Cardiovasc Res 1975 May
PMID:Glucagon-induced changes in the action potential, contraction, and Na+-K+-ATPase of cardiac muscle. 12 13

The effect of digoxin, at two different inotropic levels, was examined in normo- and hyperkalaemic dogs. For similar inotropic responses, normo- and hyperkalaemic dogs had similar levels of (Na+, K+)-ATPase inhibition and microsomal-bound digoxin.
Cardiovasc Res 1975 Jul
PMID:Dose response in vivo to digoxin in normo-and hyperkalaemia: associated biochemical changes. 12

Three sequential sets of ethanolic rats (E) and their matched controls (C) were fed regular chow containing standard vitamins with the ethanol group in each series also receiving a progressively greater alcohol intake for 3 to 6 months: E1 5%, E2 10%, and E3 25% ethanol. Electron microscopy showed swelling of mitochondria, transverse tubules and sarcoplasmic reticulum, dehiscence of intercalated discs and disintegration of myofibrils scattered throughout the ventricular myocardium in E1 and E2 as early as 7 wk after beginning 5% ethanol; in addition, there were clumping of mitochondria and supercontraction of myofibrils in E3. Concomitant with substructural abnormalities in E3, there were slight but significant depressions of cardiac myofibrillar ATPase activity and mitochondrial function. Cardiac catecholamines, hydroxyproline, and total bound glycerol were unchanged. Alteration of isometric contraction of isolated, supported left ventricular papillary muscles occurred initially in E2 and was clearly evident in E3 by significant reduction of duration of systolic active state (time from onset to peak tension), while total tension generated and peak rate of tension rise were not yet disturbed. Extra vitamin supplementation in additional rats drinking 25% ethanol minimally lessened decline in myofibrillar ATPase activity, but otherwise provided no protection. Thus, chronic daily ingestion of graded quantities of ethanol representing 10 to 30% of total calories in well-nourished animals exerted toxic effects on microstructure, metabolism and mechanics of the ventricle. These alterations are postulated to be pertinent to early pathogenesis of clinical alcoholic cardiomyopathy.
Cardiovasc Res 1975 Sep
PMID:Effects of chronic graded ethanol consumption on the metabolism, ultrastructure, and mechanical function of the rat heart. 12 56

Experimentally-induced ischaemia in the dog heart was produced by ligating the left circumflex artery. Myosin B isolated from the ischaemic portion of the myocardium differed from myosin B isolated from control tissue in its diminished response to the calcium chelator ethyleneglycol bis (beta-amino-ethylether)-N, N'-tetraacetic acid (EGTA). In the presence of EGTA, ischaemic myosin B required 2.5 +/- 0.5 min for completion of superprecipitation, whereas control myosin B required 6.6 +/- 2.5 min. Likewise, the Mg++ -activated ATPase activity of ischaemic myosin B was inhibited by EGTA to a lesser degree than control myosin B. Experiments with reconstituted myosin B using desensitized control myosin B and regulatory proteins suggest that ischaemia induces changes in the regulatory proteins (troponin and tropomyosin).
Cardiovasc Res 1976 Jan
PMID:Biochemical and morphological correlates of cardiac ischaemia: Contractile proteins. 13 Feb 6

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.
Cardiovasc Res 1976 Nov
PMID:Myocardial sarcolemmal ATPase in dogs with induced mitral insufficiency. 13 98

The possibility that the cardiac SR undergoes developmental changes at about the time of birth, and that these changes affect its ability to accumulate Ca2+ and to hydrolyse ATP has been studied. SR-rich microsomal fractions were prepared from heart muscle excised from foetal guinea pigs and rabbits 1 day before their anticipated date of birth, and from 1 day old and adult animals. For control purposes microsomes were also prepared from the relevant maternal stock animals. One day before birth the cardiac microsomes of the foetal but not of the maternal animals exhibited a decreased ability to accumulate Ca2+ by uptake but not by the binding process, and a decreased ability to hydrolyse ATP. This reduction in ATPase activity involved both the Ca2+-dependent and the Ca2+-independent ATPase enzymes. One day after birth the Ca2+-accumulating activity of the neonatal microsomes had increased, that of the rabbit via an increase in Ca2+ uptake and that of the guinea pig by an increase in Ca2+ binding. These changes were accompanied by an increase in the activity of the Ca2+-dependent ATPase. The results are interpreted to mean that the cardiac SR changes at about the time of birth, and that although the pattern of these changes may be species specific they result in an increase in the Ca2+-accumulating activity of the SR.
Cardiovasc Res 1977 May
PMID:Calcium accumulating and ATPase activity of cardiac sarcoplasmic reticulum before and after birth. 14 28

Actomyosin was extracted from myocardial homogenates from male rats of different ages of a long-inbred Fischer rat colony maintained under controlled conditions of temperature, humidity, and light. ATPase specific activity rose to a maximum at 2 months of age; this was followed by a progressive decline by about 25% at 16 months of age. However, the extractable actomyosin remained constant during this period. This loss in actomyosin ATPase specific activity is in good agreement with previously reported decrements in both stroke index and myocardial calcium content and an increase in myocardial contraction duration in aged rats.
Cardiovasc Res 1977 May
PMID:Reduced myocardial actomyosin adenosine triphosphatase activity in the ageing male Fischer rat. 14 29

The purpose of the present study was to investigate the interactions between ATP, ADP and calcium binding by rat heart sarcoplasmic reticulum vesicles (SR), and to re-evaluate the assay method used to study calcium binding. Calcium binding or transport was studied by the Millipore filtration method. Rat heart SR has an unusually high Mg2+ stimulated ATPase activity (1.37 +/- 0.16 mumol Pi per min per mg at 25 degrees C) so that previous incubation with ATP in calcium binding studies releases ADP and Pi. By maintaining ATP at high and ADP at low concentrations with an ATP-regenerating system (phosphoenolpyruvate and pyruvate kinase), calcium binding capacity was increased by two to three times that of a non-ATP-regenerating system and there was a direct relationship between the amount of Ca-binding and SR protein concentration. When Ca2+ and Mg2+ concentrations were controlled and ATP and ADP concentrations were varied independently the initial rate of Ca-binding was inhibited 25% by 1 mmol.litre-1 ADP and 48% by 3mmol.litre-1 ADP. ATP limited the initial rate of Ca-binding only at ATP levels below 2mmol.litre-1. At low ATP concentrations Ca-release was observed. However, in the presence of an ATP-regenerating system no Ca-release was observed, even at low concentrations of ATP. This study shows that ADP is an inhibitor of Ca-binding by rat heart SR. However, the possibility that high ADP concentrations in the presence of Pi from ATP hydrolysis, could facilitate calcium release cannot be excluded. In addition to the possible physiological importance, these effects must be regarded when assaying rat cardiac SR calcium binding.
Cardiovasc Res 1979 May
PMID:Effects of adenine nucleotides on calcium binding by rat heart sarcoplasmic reticulum. 15 12

An investigation of changes in the Mg2+ -dependent, Na+ -K+ -stimulated sarcolemmal ATPase and of intracellular electrolytes in the left failing heart due to pressure overload (aortic banding) was carried out in dogs. There was no change in the sarcolemmal Mg2+ -ATPase of the left or right ventricle for the whole duration (3 to 9 months) of left ventricular pressure overload. In the early phase (3 months) of aortic banding, when there was no haemodynamic evidence of left ventricular failure, there was also no significant change in the sarcolemmal Na+ -K+ -ATPase, extracellular space, or intra- and extracellular electrolytes. However, during 6 to 9 months of aortic binding when there was haemodynamic evidence of left ventricular failure (increased end-diastolic pressure, decreased cardiac index and (dP/dt)/IIP, enlarged heart), there was also a marked increase in the left ventricular sarcolemmal Na+ -K+ -ATPase and intracellular K+; and a decrease in the intracellular Na+ and Ca2+. The extracellular space in the left ventricle also increased significantly. Unlike the left ventricle, the right ventricle did not show any evidence of failure, not did it show any change in the sarcolemmal Na+ -K+ -ATPase and intracellular electrolytes during any period of aortic banding. These results suggest that the decrease in the myocardial contractility in failing heart due to pressure overload might be associated with a decrease in the intracellular Ca2+ as a result of an increase in the sarcolemmal Na+ -K+ -ATPase.
Cardiovasc Res 1979 Feb
PMID:Intra- and extracellular electrolytes and sarcolemmal ATPase in the failing heart due to pressure overload in dogs. 22 60


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