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)

Physiological and biochemical processes which take place in the nervous system at stroke and neurotrauma are reviewed, and the experience of using low doses of steroid derivatives with piridamole in the treatment of central nervous system (CNS) disorders is summarized. ATPases (including Na,K-ATPase) are reported to play an important role in CNS functioning, the correlation between Na,K-ATPase activity and the extent of CNS injury is revealed. The use of NMR-spectroscopy method for investigation of brain and spinal cord condition in vivo is suggested.
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PMID:[The role of carrier ATPases and neuromediators in neurological disorders]. 197 89

In order to evaluate the possibility of left ventricular assistance by latissimus dorsi (LD) myograft, we have studied contractile property and fatigue rates of skeletal muscle ventricle (SMV) constructed using canine LD muscles. Twenty three dogs were divided into 3 groups depending on the conditioning protocol of LD muscles; Group I (Control n = 12), Group II (Vascular delay n = 4) and Group III (Vascular delay and electrical preconditioning n = 7). SMVs in GIII dogs generated sufficient pressure and forward flow in a hydraulic test system with muscle stimulation at a burst-frequency of 50 Hz (SMV pressure 131 +/- 42 mmHg, Stroke volume 7.0 +/- 3.0 ml/beat). Although SMVs in GI and GII dogs could sustain flow for only 4.0 +/- 1.1 minutes and 32.4 +/- 14.0 minutes, respectively, SMVs in GIII were able to pump continuously for 107.5 +/- 15.0 minutes (p less than 0.01, vs GI and GII). Thermography surface temperature mapping revealed marked improvement of blood distribution of LD muscles in GII and GIII dogs. Flow rates of thoracodorsal artery during SMV stimulation were GI: 10.0 +/- 3.1 ml/minute/LD 100 g, GII: 15.0 +/- 3.7 ml/minutes/100 g and GIII: 20.7 +/- 2.5 ml/minutes/100 g (p less than 0.01 vs GI). The ratio of oxygen consumption to lactate output was GI: 0.33 +/- 0.10, GII: 0.36 +/- 0.09 and GIII: 1.56 +/- 0.97 (p less than 0.01 vs GI, p less than 0.05 vs GII). Histochemical examination of LD muscles using alkaline ATPase stain revealed muscle fiber type transformation of GIII muscles. These results suggest electrically preconditioned LD muscles have sufficient contractile property for partial left ventricular assistance, and highly fatigue-resistant properties resulted from muscle fiber transformation, improved muscle perfusion and metabolic changes.
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PMID:[Potential for left ventricular assistance by latissimus dorsi myograft--sequential effects of electrical preconditioning on skeletal muscle fiber type, blood flow and metabolic status]. 205 Oct 85

In order to study the mechanochemical coupling in actomyosin energy transduction, the sliding distance of an actin filament induced by a myosin head during one ATP hydrolysis cycle was obtained using an in vitro movement assay, which permitted quantitative and simultaneous measurements of (1) the movements of single fluorescently-labeled actin filaments on myosin bound to coverslip surfaces and (2) the ATPase rates. The sliding distance was determined as (the working-stroke time in one ATPase cycle, Tws) x (the filament velocity, v). The working-stroke time (Tws) was obtained from the ATPase turnover rate of myosin during the sliding (kT), the ATP hydrolysis time on myosin heads (delta T) and the ON-rate at which myosin heads enter into the working-stroke when they encounter actin (kON); Tws approximately 1/kT-delta T-1/kON. kON was estimated by analyzing the movements of very short (40 nm) filaments. The resulting sliding distance during one ATP hydrolysis cycle near zero load was greater than 100 nm, which is about 10 times longer than that expected for a single attachment-detachment cycle between an actin monomer and a myosin head. This leads to the conclusion that the coupling between the chemical and mechanical reactions is not rigid in a one to one fashion.
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PMID:Loose coupling between chemical and mechanical reactions in actomyosin energy transduction. 208 30

The purpose of this study was to determine the extent to which functional demand regulates the biochemical character and enzyme capacities of the rat myocardium. Hearts from donor rats were heterotopically transplanted onto the abdominal aorta and inferior vena cava of isogenic recipients. The procedure results in a perfused but nonpumping heart that has a reduced heart rate (HR) and performs essentially no stroke work (SW). After 30 days, metabolic enzyme activities (phosphorylase, 6-phosphofructokinase, citrate synthase, and 3-hydroxyacyl-CoA dehydrogenase) were significantly lower (40-60%) in the nonworking heart. Specific sarcoplasmic reticulum Ca2(+)-adenosinetriphosphatase (ATPase) activity was unchanged, but activity per gram of heart was 41% lower. Myosin isozymes were 58% V1, 21% V2, and 21% V3 in the nonworking heart compared with 100% V1 in the working heart. Myosin and myofibrillar ATPase activities each decreased by 28%. These findings suggest that both HR and SW play major and specific roles in regulating myocardial biochemical capacities and determining the myosin phenotype.
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PMID:Role of cardiac work in regulating myocardial biochemical characteristics. 214 21

Effects of carbacyclin, a synthetic analogue of prostacyclin on Na, K-ATPase, Ca, Mg- and Ca-ATPase activity of plasmatic membrane (PM) and sarcoplasmic reticulum (SR) of the heart normotensive (WKY) and stroke-prone spontaneously hypertensive (SHR-SP) rats were examined. In SR carbacyclin was found to increase Ca, Mg- and Ca-ATPase activity in SHR-SP and decrease the activity of this enzymes in WKY. Carbacyclin caused identical effect on ATPase activity in PM in WKY and SHR-SP, but the greatest effects were in WKY.
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PMID:[The effect of carbacyclin on the ATPase activity in the heart of normotensive and spontaneously hypertensive rats with a hereditary susceptibility to stroke]. 214 5

In order to study the mechanochemical coupling in actomyosin energy transduction, the sliding distance of an actin filament induced by one ATP hydrolysis cycle was obtained by using an in vitro movement assay that permitted quantitative and simultaneous measurements of (1) the movements of single fluorescently labeled actin filaments on myosin bound to coverslip surfaces and (2) the ATPase rates. The sliding distance was determined as (the working stroke time in one ATPase cycle, tws) x (the filament velocity, v). tws was obtained from the ATPase turnover rate of myosin during the sliding (kt), the ATP hydrolysis time (delta t) and the ON-rate at which myosin heads enter into the working stroke state when they encounter actin (kON); tws approximately 1/kt-delta t-1/kON. kt was estimated from the ATPase rates of the myosin-coated surface during the sliding of actin filaments. delta t has been determined as less than 1/100 per second, kON was estimated by analyzing the movements of very short (40 nm) filaments. The resulting sliding distance during one ATP hydrolysis cycle near zero load was greater than 100 nm, which is about ten times longer than that expected for a single attachment-detachment cycle between an actin and a myosin head. This leads to the conclusion that the coupling between the ATPase and attachment-detachment cycles is not determined rigidly in a one-to-one fashion.
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PMID:Mechanochemical coupling in actomyosin energy transduction studied by in vitro movement assay. 214 98

We have recently demonstrated that K(+)-induced dilation of cerebral resistance-sized vessels has two independent components, only one of which seemed sodium pump dependent. In our current investigation, potassium-induced dilation of spontaneous tone was compared in cerebral arteries from normotensive Wistar-Kyoto rats and age-matched stroke-prone spontaneously hypertensive rats. Branches of the posterior cerebral artery were cannulated and pressurized, and these vessels developed spontaneous tone. After a 5-minute period in K(+)-free physiological saline solution, K+ was increased in 1-mM increments to a final concentration of 15 mM. In the normotensive arteries, K+ concentrations between 0 and 5 mM K+ resulted in dilations that had a transient (sodium pump-dependent) component, and K+ concentrations in excess of 7 mM produced dilations that lacked a transient (sodium pump-independent) component. Similar branches from the hypertensive rat also responded with transient dilations to K+ (less than 5 mM), and these were significantly greater at 3 mM K+. However, the maintained dilations to K+ (greater than 7 mM), noted in preparations from Wistar-Kyoto rats, were absent in seven of eight preparations. Thus, the impaired dilations, in the hypertensive vessels, to K+ described here is a consequence of altered function of some sodium pump-independent component rather than altered Na+,K(+)-ATPase activity.
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PMID:Impaired potassium-induced dilation in hypertensive rat cerebral arteries does not reflect altered Na+,K(+)-ATPase dilation. 217 51

Rapid regulation of relaxation is essential to allow the heart to alter stroke volume in response to stress. Inasmuch as Ca2+ transport by the sarcoplasmic reticulum (SR) is an important determinant of relaxation, the purpose of this study was to examine developmental differences in the ability of isoproterenol to alter relaxation time and to determine if these differences were associated with age-related changes in Ca2+ transport by the SR in isolated, perfused adult and newborn guinea pig hearts. Control values of the time constant of isovolumic relaxation (tau) were 37.8 +/- 5.9 ms in adult hearts (n = 8) and 31.6 +/- 5.3 ms in newborn hearts (n = 6). With maximum isoproterenol stimulation, the decrease in tau was significantly greater in adult (51.1 +/- 8.8%, mean +/- SD) compared with that in newborn (26.3 +/- 3.1%, P less than or equal to 0.0001) hearts. Ca2+ uptake, Ca2(+)-dependent adenosinetriphosphatase activity, and Ca2+ pump density were all significantly greater in SR vesicles isolated from adult hearts compared with values measured in SR vesicles from newborn hearts. We conclude that developmental differences in the capacity of the SR to sequester Ca2+ may contribute to age-related differences in the functional response of the heart to isoproterenol.
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PMID:Age-related changes in myocardial relaxation and sarcoplasmic reticulum function. 238 15

Subarachnoid hemorrhage was produced experimentally in cats by intracisternal injection of non-heparinized autologous arterial blood obtained by cardiac puncture under ketamine and xylazine anesthesia. Cats were sacrificed at varying time intervals between 30 min and 7 days post ictus. Measurements of resting membrane potential were recorded from smooth muscle cells of the basilar artery. These measurements were obtained by impalement from the adventitial surface of isolated but otherwise intact segments of the artery using glass microelectrodes with tip sizes less than 0.1 micron. The resting membrane potential recorded in vitro from animals previously subjected to subarachnoid hemorrhage in vivo was consistently and significantly depolarized when compared to normal controls. This depolarization was present as early as 30 min post ictus. Addition of the cardiac glycoside, ouabain, in a concentration of 10(-5)M depolarized cells from both control and experimental animals. There is a significant electrogenic pump potential contribution to the resting membrane potential of vascular smooth muscle cells. Ouabain is a potent blocker of Na+, K+-ATPase, the enzyme responsible for maintaining the cation electrochemical gradients. The depolarization recorded in these cells following subarachnoid hemorrhage is not, therefore, due to impairment of the electrogenic pump. The significance and implications of these findings are discussed.
Stroke
PMID:Altered membrane properties of cerebral vascular smooth muscle following subarachnoid hemorrhage: an electrophysiological study. I. Changes in resting membrane potential (Em) and effect on the electrogenic pump potential contribution to Em. 241 49

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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