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)

Previous studies in hearts of female rats have demonstrated that ventricular hypertrophy due to systolic overload, when combined with hypertrophy induced by a chronic swimming program, results in increased cardiac performance and enhanced contractile protein activity compared with the effects of hypertension alone. To explore how a chronic running program affects the function of hypertensive hearts, renal hypertension was created in female rats, and the animals were subjected to a program of chronic treadmill running. Running alone caused enhanced cardiac function, an increase in myosin adenosinetriphosphatase (ATPase) activity, and an increase in the percent of the V1 myosin isoenzyme. Hypertension alone caused cardiac hypertrophy with a depression in myosin ATPase activity and a decrease in the percent of the V1 isoenzyme. Running improved cardiac function in hearts of normotensive rats but had no effect in hearts of hypertensive rats. Despite the diminished myosin ATPase activity in hearts of hypertensive runners and the decrease in percent of the V1 isoenzyme, cardiac function was well maintained. The results demonstrate that a chronic running program in hypertensive rats, in contrast to a chronic swimming program, had virtually no effect on cardiac performance or contractile proteins. The dissociation between myocardial performance and the contractile proteins implicates other biochemical mechanisms in the adaptations observed.
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PMID:Combined effects of hypertension and chronic running program on rat heart. 295 51

In most animal species, left ventricular hypertrophy due to pressure overload is associated with an advantageous increase of the "slow" V3 isomyosin. In contrast, in spontaneously hypertensive turkeys, the development of left ventricular hypertrophy is associated with the synthesis of a "fast" V1-like isomyosin, with high incidence of cardiac failure. This could be related to the high catecholamine levels found in these animals. This is why we studied the ventricular myosin pattern after lowering of blood pressure and regression of cardiac hypertrophy obtained by means of labetalol, and alpha- and beta-blocking drug which inhibits the effects of catecholamines. From the 2nd to the 32nd week of age, 22 turkeys were treated with increasing doses of p.o. labetalol (from 20 to 35 mg/kg body weight daily) and 16 other turkeys were given daily p.o. placebo. Blood pressure and heart rate were periodically measured by an indirect method. After sacrifice, the degree of cardiac hypertrophy was evaluated by the biventricular weight to body weight ratio, ventricular myosin was purified, Ca++-activated ATPase activity assessed, and ventricular myosin pattern was determined by two-dimensional gel electrophoresis of myosin heavy chains. Plasma and cardiac catecholamines were measured by high performance liquid chromatography. Throughout the study period, blood pressure and heart rate were significantly reduced in the labetalol-treated animals as compared to the untreated ones. At the end of the study period, the ventricular mass was significantly lower in the labetalol group. Nevertheless, no differences were observed in ventricular myosin pattern and Ca++-activated ATPase activity levels between the two groups. In the labetalol group, an increase in plasma catecholamines and only a slight, but not significant, increase in cardiac catecholamines was found. These data indicate that in spontaneously hypertensive turkeys, the synthesis of the "fast" V1-like isomyosin is not influenced by known pathophysiological stimuli like blood pressure, cardiac hypertrophy and catecholamines.
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PMID:Ventricular myosin pattern of spontaneously hypertensive turkeys is unaffected by labetalol treatment. 297 Aug 41

The myofibrillar ATPase activity and pyrophosphate gel electrophoretic pattern of native myosin of fresh human left ventricular papillary muscles were examined in 52 cases of mitral valve replacement. The myofibrillar ATPase activity of hypertrophied myocardium did not differ from that of non-hypertrophied myocardium (mean +/- SD, 36.2 +/- 8.7 vs 31.8 +/- 8.6 nmolPi/mg/min, ns) and there was no significant difference in myofibrillar ATPase activity as a function of left ventricular enddiastolic pressure. Pyrophosphate gel electrophoresis of myosin revealed the presence of two components. It is questionable whether the component of higher electrophoretic mobility (approximately 25-35% in concentration) is identical with rat ventricular myosin VM-1 because an increase in this component seems to correlate with a decrease of myofibrillar ATPase activity, its concentration was significantly higher in the hearts with left ventricular hypertrophy, high enddiastolic pressure, high aortic pressure or low cardiac index. From these results, it is not necessarily clear whether hemodynamic overload in valvular heart diseases can alter left ventricular myofibrillar ATPase activity, but it can be said that the overload influences the concentration of the two components of native myosin revealed by pyrophosphate gel electrophoresis.
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PMID:Relationship between the myofibrillar ATPase activity of human biopsy material and hemodynamic parameters. 300 96

Effects of myocardial hypertrophy caused by pressure overload on sarcolemmal Na+,K+-ATPase and positive inotropic action of strophanthidin were examined in cats. Partial ligation of the main pulmonary artery for four weeks resulted in right ventricular hypertrophy with no significant changes in left ventricular muscle. Hypertrophy was associated with a reduction in the number of active Na+,K+-ATPase units. Affinity of the remaining enzyme for [3H]ouabain was unchanged. No apparent right or left shift in dose-response curve for the positive inotropic effect of strophanthidin was observed and toxic concentrations of strophanthidin were unchanged; however, the degree of the positive inotropic effect produced by high concentrations of strophanthidin was significantly smaller in hypertrophied muscle. Moreover, decreases in developed tension rather than tachyarrhythmias was the predominant form of toxicity observed in hypertrophied muscle. These results indicate that myocardial hypertrophy reduces the number of active Na+,K+-ATPase units per milligram protein, decreases maximal positive inotropic effect of strophanthidin, and alters the prevailing form of strophanthidin toxicity.
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PMID:Pressure-induced cardiac hypertrophy: changes in Na+,K+-ATPase and glycoside actions in cats. 303 78

The activity of the Na-K pump was assessed in normal and hypertrophied isolated feline myocytes by measuring ouabain-sensitive 42-K uptake. Right ventricular hypertrophy was produced in feline myocardium by placing a constricting band around the pulmonary artery of adult cats. High yields of calcium tolerant myocytes were isolated from the right and left ventricle of banded and sham operated animals. Intracellular sodium (Na) and potassium (K) concentrations (mM) were not significantly different (P greater than 0.5) in normal (Na: 13.2; K: 133.4) and hypertrophied (Na: 12.3; K: 127.5) myocytes. Morphometric analysis demonstrated a 26% increase in width and a 42% increase in volume of hypertrophied myocytes, however, the sarcomere length (1.9 mu) was not different in both cell types. The rate constant (k, min-1) describing 42-K uptake and the calculated total K influx (I, pmol/cm2/sec) were not significantly different (P greater than 0.5) in normal (k = 0.059; I = 15.9) and hypertrophied (k = 0.062; I = 15.3) cells. Ouabain-sensitive (active) K influx, a measure of Na-K pump activity, was maximally inhibited at 10(-4)M ouabain in both cell types. At this concentration, ouabain-sensitive K uptake was decreased 23.5% in hypertrophied myocytes compared to control. The decrease in active K influx may be due to a decrease in the activity of the Na-K ATPase and/or to a reduction in the passive movement of sodium and potassium down their electrochemical gradients.
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PMID:Decreased sodium-potassium pump activity in isolated hypertrophied feline ventricular myocytes. 316 Sep 4

The effects of isoprenaline administration (300 micrograms/kg for 5 weeks) on rat soleus muscle capillarity and glycolytic and oxidative capacities were evaluated. The treatment resulted in ventricular hypertrophy. The activities of lactic dehydrogenase, pyruvate kinase, citrate synthase, and cytochrome c oxidase in soleus muscle homogenates were not different between control and isoprenaline-injected animals. Capillaries were visualized in muscle cross sections treated to demonstrate ATPase activity after acid preincubation. Capillary density was higher in the experimental (873 +/- 38 capillaries/mm2) than in the control (713 +/- 33 capillaries/mm2) animals. Capillary to fiber ratio was also higher in the experimental (2.47 +/- 0.10) than in control (2.09 +/- 0.08) animals, but fiber cross-sectional area was not changed by the treatment (2836 +/- 87 microns2 in controls and 2951 +/- 136 microns2 in experimental). A plot of capillary to fiber ratio vs. fiber cross-sectional area showed that at a given fiber cross-sectional area the value of capillary to fiber ratio of the treated animals was higher than that of the controls. This indicates that treatment resulted in the proliferation of microvessels. The results suggest that prolonged beta-adrenergic stimulation results in the development of new capillaries but that this is not accompanied by increases in the oxidative capacity of the soleus muscle of the rat.
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PMID:Long-term isoprenaline administration produces an increase in capillarity in the soleus muscle of the rat. 358 Sep 52

A decrease in cardiac function and intracellular calcium, and an increase in cardiac sarcolemmal ATPase have been reported in experimentally induced aortic stenosis of 6 to 9 months duration. Prazosin has been used in the treatment of heart failure due to mechanical ventricular overload. It is, however, not known whether prazosin treatment gives only hemodynamic benefit with accompanying subjective improvement or if it also improves the condition of the myocardium in terms of contractility and biochemical changes. The present investigation deals with the effects of 3 months of prazosin treatment on cardiac function, electrolytes, and ATPase in dogs with aortic stenosis of 3 months duration. Although there were no significant changes in most of the left and right ventricular hemodynamic parameters, the left ventricular end-diastolic pressure increased significantly after 3 months of aortic stenosis. Prazosin prevented further deterioration of cardiac function. All the dogs developed left ventricular hypertrophy and all chest X-rays showed cardiomegaly. Concomitant with these changes, there was a tendency towards a decrease in total tissue Ca++ and intracellular Ca++ and K+ and a tendency towards an increase in sarcolemmal Na+-K+-ATPase. Prazosin treatment, although it markedly reduced left ventricular end-diastolic pressure, did not reduce the cardiomegaly. There were no significant changes in any of the other hemodynamic parameters. Prazosin treatment decreased sarcolemmal ATPase and tended to increase intracellular Ca++. It appears therefore that prazosin not only tends to bring the cardiac function towards control values but also tends to correct the ATPase and intracellular Ca++ levels of the failing heart.
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PMID:Effect of prolonged prazosin treatment on hemodynamic and biochemical changes in the dog heart due to chronic pressure overload. 608 30

Hypertension and resulting left ventricular hypertrophy was induced in young male Wistar rats (60 to 70 days old) by narrowing of one renal artery (Goldblatt II). 8 and 24 weeks after operation, myocardial oxygen consumption was measured on a modified in situ heart-lung preparation with nearly isovolumetric left ventricular contractions. Measured myocardial oxygen consumption was related to left ventricular wall stress. The myosin isoenzyme pattern of each heart was determined with pyrophosphate gel electrophoresis. Oxygen consumption related to wall stress averaged over the entire heart cycle amounted to 15 mumoles O2/g X min 8 weeks after operation, and 24.4 mumoles O2/g X min in age-matched controls (delta 38%, p less than 0.0005). When wall stress was averaged over systole, oxygen consumption of the hypertrophied hearts amounted to 0.112 mumoles O2/g x beat, and 0.149 mumoles O2/g x beat in the controls (delta 25%, p less than 0.05). The proportion of VM-3 (the cardiac myosin isoenzyme of lowest ATPase activity) increased from 26.3% in the controls to 30.1% in the Goldblatt hearts (delta 14%, n.s.). 24 weeks after operation, oxygen consumption related to wall stress averaged over the entire heart cycle amounted to 16.1 mumoles O2/g x min, in age-matched controls 20.5 mumoles O2/g x min (delta 21%, p less than 0.05). When wall stress was averaged over systole, oxygen consumption of the Goldblatt hearts amounted to 0.080 mumoles O2/g x beat, and in the controls 0.107 mumoles O2/g x beat (delta 25%, p less than 0.0005). The proportion of VM-3 increased from 33.5% in the controls to 43.2% in the hypertrophied hearts (delta 29%, p less than 0.05). The present findings indicate that the reduced oxygen consumption of the pressure-loaded heart should be attributed to a redistribution of myosin isoenzymes. The transformation of myocardium into a slower, but more efficiently working muscle due to an increase in VM-3 can be interpreted as an adaptational process.
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PMID:Alterations in cardiac oxygen consumption under chronic pressure overload. Significance of the isoenzyme pattern of myosin. 621 50

A decrease in the cardiac function and intracellular calcium, and an increase in the cardiac sarcolemmal ATPase have been reported in aortic stenosis of 6 to 9 months duration in dogs. The present investigation deals with the effect of 3 months of digoxin treatment on cardiac function, electrolytes and ATPase in dogs with 3 months of aortic stenosis in order to determine whether digoxin treatment gives only haemodynamic improvement or if it also improves the condition of the myocardium in terms of contractility and biochemical changes. There were no significant changes in any of the haemodynamic parameters of left and right ventricles except the left ventricular end-diastolic pressure which increased significantly at 3 months of aortic stenosis. All the hearts developed left ventricular hypertrophy. Concomitant with these changes, there was a tendency for a decrease in the total tissue Ca2+, intracellular Ca2+ and K+, and a tendency for an increase in the sarcolemmal ATPase. There were no significant differences in any of the haemodynamic parameters between the aortic stenotic and digoxin treated aortic stenotic dogs indicating that digoxin was at least maintaining the haemodynamics close to the pretreatment level. Although digoxin treatment prevented the changes in the sarcolemmal ATPase and extracellular space, it did not prevent the further decrease in the total or intracellular Ca2+. The total and intracellular Ca2+ was still significantly higher than previously observed after 6 to 9 months of aortic stenosis. These results suggest that digoxin treatment not only tended to prevent further deterioration of cardiac function but also tended to prevent further changes in the sarcolemmal ATPase and electrolytes.
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PMID:Effect of chronic digoxin treatment on cardiac function, electrolytes and ATPase in failing heart due to pressure overload. 623 15

This paper reports the following data with regard to the BBWT cardiovascular system: 1) Arterial Blood pressure progressively increases from 1 to 12 month of age, accompanied by marked left ventricular hypertrophy; 2) The myosin ATPase activity is enhanced about three times; 3) No differences in myosin light chain pattern is observed; 4) The peptide pattern obtained after chymotryptic digestion of the myosin molecule shows that some peptides, which are not evident or barely discernible, in 1 month old animal, are present in the adult one. These findings are surprising because it is well known that the ATPase activity decreases with age and hypertrophy. It is possible that other factors, as the levels of circulating cathecolamines or the thyroid hormones, are involved in the control of myosin synthesis and consequently in its ATPase activity.
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PMID:Changes in ventricular myosin properties during broad breasted white turkey (BBWT) development. 645 20


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