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)

1. For many years it has been known that when muscles are depolarized by raising [K(+)](out) there is an increase in respiration, even at levels of depolarization below the threshold for a detectable contracture.2. K(+)-stimulated respiration occurs in muscles in which protein synthesis is blocked with puromycin. Stimulation does not depend upon activation of phosphorylase kinase. In muscle poisoned with IIA and kept in N(2), depolarizations below the threshold for contracture cause a fall in creatine phosphate. Apparently an ATPase is activated by depolarization; the resulting ADP is probably the trigger for the increase in oxygen uptake.3. When the T-tubules are destroyed by the glycerol-osmotic shock method depolarization does not produce an increase in respiration.4. Caffeine is known to stimulate respiration at concentrations below the threshold for producing a contracture. Muscles that have been made refractory to stimulation by potassium are still stimulated by caffeine: the action of caffeine is not antagonized by an increase in extracellular Mg(2+). Caffeine must act on a later step in excitation-contraction coupling.5. K(+)-stimulated respiration ultimately depends on the presence of Ca(2+) in the Ringer. However, the Ca(2+) can be replaced by Ni(2+). It is known that Ni(2+) does not activate actomyosin. Ni(2+) is not sequestered by isolated fragments of the sarcoplasmic reticulum. It seems that the Ni(2+) or Ca(2+) in the extracellular solution is required for a superficial step in excitation-contraction coupling.6. Respiration is also often stimulated when muscles are placed in an isotonic sucrose solution, even though the fibres are hyperpolarized. A trace amount of Ca(2+) in the sucrose solution is probably necessary for the response.7. An interaction between Ca(2+) and a superficial membrane receptor appears to be an essential, early step in excitation-contraction coupling.
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PMID:The steps between depolarization and the increase in the respiration of frog skeletal muscle. 424 10

Two dogs were diagnosed as malignant hyperthermia susceptible based on increased susceptibility (P less than 0.001) of biopsied muscle to caffeine-induced contracture. Erythrocytes from malignant hyperthermia and normal dogs were then examined for an antioxidant system deficiency. Values for serum muscle enzymes, reticulocytes and corpuscular hemoglobin were mildly elevated. Osmotic fragility was increased: hemolysis occurred at a NaCl concentration 10 mM higher than for normal dogs (P less than 0.001). A 35% glucose-6-phosphate dehydrogenase deficiency (P less than 0.001) with a 40% compensatory increase (P less than 0.01) in 6-phosphogluconate dehydrogenase activity was found. The membrane Ca2+-activated ATPase activity was abnormal: 100% increased with a 40% decreased Arrhenius activation energy (P less than 0.005) and increased thermostability. A 40% increased intracellular accumulation of total Ca2+ occurred in response to in vitro energy depletion in erythrocytes from one malignant hyperthermia dog (P less than 0.01). The multifactorial pattern of inheritance and the broad spectrum of malignant hyperthermia susceptibility are proposed to result from an antioxidant system deficit unmasking or aggravating an intrinsic muscle membrane anomaly. An individual from a family with a history of malignant hyperthermia or unexplained anesthetic death should be considered malignant hyperthermia susceptible if erythrocyte osmotic fragility is abnormal and there is a mild, unexplained elevation in serum creatine kinase.
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PMID:Canine malignant hyperthermia susceptibility: erythrocytic defects--osmotic fragility, glucose-6-phosphate dehydrogenase deficiency and abnormal Ca2+ homeostasis. 615 Jul 53

Using slices of mouse or rat cerebral cortex incubated with [3H]adenosine or [3H]adenine and/or [14C]GABA we have examined factors affecting the release of these compounds, and especially the influence of methylxanthines. Although release of purines and GABA could be induced by ouabain (10(-4) M), or p-hydroxymercuribenzoate (5 x 10(-4) M) no release was produced by ethacrynic acid (10(-3) or 10(-4) M) phenytoin (10(-3) M), noradrenaline or SC 13504. Release is probably not therefore related to (Na+, K+) ATPase or Mg2+-ATPase inhibition. At concentrations of 10(-3) and 10(-4) M, caffeine, theophylline, aminophylline and isobutyl-methylxanthine (IBMX) markedly depressed the release of purines evoked by ouabain. Non-xanthine inhibition of phosphodiesterase had much weaker though statistically significant effects. The methylxanthines had no significant effect on GABA release. It is suggested that the results can be explained on the basis of a positive feedback system in which released adenosine activates membranal adenylate cyclase, and the increased concentration of cyclic AMP which results form or origin of much of the adenosine released subsequently. However, we cannot exclude the existence of an intracellular receptor for methylxanthines which causes directly the inhibition of purine release.
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PMID:Methylxanthines modulate adenosine release from slices of cerebral cortex. 616 26

In order to investigate the mechanism of skeletal muscle relaxation induced by dimethyl sulfoxide, 2-butoxyethanol and dimethyl sulfoxide were examined for their effects on 1) Ca2+ uptake into and efflux from sarcoplasmic reticulum vesicles prepared from rabbit fast skeletal muscle and crayfish tail muscle by the murexide method, 2) ATPase activities of rabbit reticulum vesicles, 3) the isolated phrenic nerve-diaphragm preparation of the rat and 4) crayfish opener muscle preparation. Ca2+ efflux rate from rabbit reticulum vesicles was markedly decreased with increasing concentrations (5-20% v/v) of dimethyl sulfoxide without affecting the maximum Ca2+ uptake by the reticulum. 2-Butoxyethanol showed quite contrary effects. Dimethyl sulfoxide strongly inhibited the activity of basal ATPase rather than of Ca2+-dependent ATPase. 2-Butoxyethanol did not significantly inhibit the activity of basal ATPase, but markedly increased Ca2+-dependent ATPase activity. Antagonisms between dimethyl sulfoxide and caffeine were demonstrated either in contractions of crayfish opener muscles or in the Ca2+ release from crayfish sarcoplasmic reticulum vesicles. These results indicate a possibility that dimethyl sulfoxide reversibly induces skeletal muscle relaxation mainly in the sarcoplasmic reticulum by means of decreasing the rate and the amount of Ca2+ release from the reticulum.
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PMID:Modification of calcium fluxes by dimethyl sulfoxide and 2-butoxyethanol in sarcoplasmic reticulum vesicles: a possible mechanism for skeletal muscle relaxation induced by dimethyl sulfoxide. 621 58

The characteristics of Ca2+ release in relation to Ca2+ binding were studied in sarcoplasmic reticulum vesicles isolated from canine myocardium. The Ca2+ binding appeared to be dependent on ATP as a 4 fold increase in Ca2+ binding was observed upon the addition of ATP. In the presence of a suboptimal ATP concentration (20 mumol/l; without ATP regenerating system) a rapid release of Ca2+ started within 2 min. The rate of Ca2+ release was increased by increasing the concentration of Ca2+ in the preincubation medium when studied by diluting preloaded vesicles in medium free of Ca2+ and ATP; an apparent saturation was reached at 5 mmol/l Ca2+ but Ca2+ release again increased between 5 and 10 mmol/l Ca2+. High pH (8.0) enhanced the Ca2+ release process. When Ca2+ loaded vesicles were treated with various phospholipases and proteases, an enhanced Ca2+ release was observed in comparison to the control values. The release of Ca2+ was also increased by pharmacological agents like caffeine, ether and halothane. The Ca2+ release rate was stimulated by the p-chloromercurybenzoate treatment, which decreased ATP dependent Ca2+ binding and Ca2+-stimulated ATPase activities of the sarcoplasmic reticulum vesicles. The effect of temperature when evaluated by Arrhenius plots showed a higher energy of activation of Ca2+ release (66.15 kJ/mol) in comparison to that for Ca2+ binding (41.03 kJ/mol). These results indicate that, although Ca2+ release and Ca2+ binding activities of the cardiac sarcoplasmic reticulum appears to be related, Ca2+ release is probably a distinct process and is controlled differently. It seems that the Ca2+ release site in sarcoplasmic reticulum membranes is lipoprotein in nature.
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PMID:Characterization of Ca2+ release from the cardiac sarcoplasmic reticulum. 623 29

A Ca-selective electrode was used to study the effect of caffeine on different fractions of sarcoplasmic reticulum membranes of rabbit skeletal muscles. Caffeine was found to uncouple Ca2+ transport and ATP hydrolysis in a fraction, which is enriched with fragments of terminal cisterns according to the electron microscopy data. Caffeine does not produce any effect on the light fraction containing no fragments of terminal cisterns. It is concluded that caffeine-sensitive Ca2+-dependent ATPase is localized in terminal cisterns of the sarcoplasmic reticulum.
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PMID:[Intracellular localization of the caffeine-sensitive form of Ca-dependent ATPase in the sarcoplasmic reticulum]. 623 92

The kinetics of influx and efflux of 45Ca and its accumulation by the subcellular membranes of adipose tissue have been studied. The initial rate of Ca2+ efflux does not depend on the intracellular concentration of Na+ and K+. The rate of exchange between intracellular 45Ca and 40Ca of the incubation medium is independent on concentration of Na+ and K+ in the incubation mixture. This suggests the absence of Na,Ca-transmembrane exchange in the adipocytes. The changes in the ratio of intracellular concentration of Na+ and K+ by the factors inhibiting the activity ofNa,K-ATPase cause redistribution of Ca in the intracellular pools of the adipocytes. The lypolytic agents (adrenalin, adrenocorticotropic hormone, caffeine) but not dibutytyl-3' : 5'-AMP, accelerate Ca2+ efflux from the adipocytes. At physiological concentrations of ATP, succinate and Pi the highest Ca-accumulating activity is observed in adipose tissue mitochondria. The highest initial rate of Ca uptake, as in the case of contractile tissues, is detected in the endoplasmic reticulum membranes. In contrast to the plasma membranes and reticulum, in which the Ca-accumulating capacity is independent of ATP concentration up to 0.5 mM, the Ca-accumulating capacity of mitochondria decreases 8--9-fold with a reduction in ATP concentration from 4 down to 1 mM. The physiological significance of this phenomenon in the action mechanism of lipolytic agents, which reduce the ATP content in the adipocytes, is discussed.
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PMID:[Mechanisms of regulation of intracellular distribution of Ca2+ in adipose tissue]. 624 69

1. In fibroblastic L cells, spontaneously repeated hyperpolarizing responses (oscillation of membrane potential) and hyperpolarizing responses evoked by electrical stimuli were suppressed by the external application of a K(+) channel blocker, nonyltriethylammonium (C(9)). This hydrophobic TEA-analogue also inhibited the hyperpolarization induced by intracellular Ca(2+) injection.2. Quinine or quinidine, known inhibitors of the Ca(2+)-activated K(+) channel of red cells, instantaneously inhibited these hyperpolarizations. Thus, these hyperpolarizations are likely to be caused by the operation of Ca(2+)-sensitive K(+) channels.3. Azide, which is known to inhibit the mitochondrial Ca(2+) uptake in fibroblasts, and caffeine, dantrolene Na and oxalate, which affect the microsomal Ca(2+) transport, did not exert any effects upon the electrical potential profiles.4. On the other hand, Ca(2+) channel blockers (nifedipine, D 600 and Co(2+)) suppressed the hyperpolarizing responses, but not the hyperpolarizations produced by intracellular Ca(2+) injection, suggesting that the calcium ions responsible for the hyperpolarizing responses are mainly derived from outside the cell through Ca(2+) channels.5. Flavones of plant origin, which are known to inhibit Ca(2+)-ATPase, prolonged the duration of the hyperpolarizing phase of the oscillation or produced a sustained hyperpolarization.6. It is concluded that the Ca(2+) channel and the Ca(2+) pump play essential roles in the generation of the hyperpolarizing response and of the membrane potential oscillation in L cells, and that these hyperpolarizations are brought about by a transient elevation of cytosolic Ca(2+) level which, in turn, activates Ca(2+)-dependent K(+) channels.
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PMID:Calcium channel and calcium pump involved in oscillatory hyperpolarizing responses of L-strain mouse fibroblasts. 628 29

The increased rate of Ca2+ uptake and ATPase activity in isolated cardiac sarcoplasmic reticulum (SR) by adenosine 3',5'-monophosphate (cAMP) has been shown to be activated by a cAMP-dependent protein kinase (cAMP kinase). Functionally skinned myocardial fiber preparations were used to study the mechanisms of cAMP action on the SR at the same time that tension was monitored. cAMP effects were studied on Ca2+ -activated tension of the contractile proteins, and on Ca2+ uptake and release from the SR using caffeine-induced tension transients. Neither cyclic AMP (0.1-5 microM) nor the catalytic subunit of cAMP kinase (0.1-1 microM) (PK-C) significantly changed either the maximal or the submaximal Ca2+ -activated tension. The areas of the tension transients were unchanged when cAMP was present in the releasing solution (release phase), and were significantly increased up to a mean of about 80% when cAMP or PK-C was present in the Ca2+ loading solutions (uptake phase). The increased tension transient was blocked by heat-stable inhibitor of cAMP kinase. We conclude that cAMP-induced increases in Ca2+ uptake by the SR could play an important role in the positive inotropic effect. cAMP kinase could thus play a crucial role in the regulation of myocardial contractility.
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PMID:Mechanism of adenosine 3',5'-monophosphate (cAMP)-induced increase in Ca2+ uptake by the sarcoplasmic reticulum in functionally skinned myocardial fibers. 628 52

Both calcium ++-activated magnesium++ adenosine triphosphatase and the calcium++-accumulating activity of SR isolated from white skeletal muscle of pigs of the Yorkshire breed resistant to MH and pigs of the Belgian Landrace breed susceptible to MH continue to be stable throughout the process of growth. There was not any detectable difference between the two breeds and therefore it could not be concluded that there was a defective SR membrane. Abnormal contractions induced by halothane and caffeine in biopsy specimens of muscle of MH-susceptible pigs of the Belgian Landrace breed are mainly produced by external calcium++, CN--not having any inhibitory effect in these cases. The contractions induced by combined caffeine and halothane in susceptible animals are more marked than those occurring in resistant animals. These increased contractions are mainly due to external Ca++ and, to a less extent, to CN--sensitive mitochondrial Ca++ fluxes.
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PMID:[Halothane-induced malignant hyperthermia (MH) in the Belgian Landrace breed of pigs: some findings concerning the role of subcellular fractions (author's transl)]. 644 58


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