Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasodilator responses to acute intra-arterial infusions of K+ are attenuated in dogs with chronic one-kidney perinephritic hypertension in rats with chronic two-kidney Goldblatt hypertension, and in men with essential hypertension. There is evidence that K+ evokes vasodilation by stimulating vascular smooth muscle membrane Na+-K+-activated adenosine triphosphatase, thereby increasing activity of the cellular Na+-K+ electrogenic pump. We therefore proposed that there may be an underlying decrease in the operation of this pump in vascular smooth muscle of hypertensives. The operation of the cellular Na+-K+ pump may be estimated by measurement of rubidium uptake. Thus, so further investigate our hypothesis, we measured 86Rb uptake in small mesenteric arteries and splanchnic veins from 12 dogs with chronic uncomplicated one-kidney perinephritic hypertension and from 12 normotensive control dogs. Vessels were excised under thiamylal anesthesia and incubated in cold medium (plasma or Krebs-Henseleit solution) for sodium loading and then the velocity of 86Rb uptake was estimated in the absence of or in the presence of ouabain, a specific inhibitor of the Na+-K+ pump. In neither arteries nor veins was there evidence for differences between hypertensives and normotensives in the ouabain-insensitive uptake of 86Rb. In contrast, the ouabain-sensitive 86Rb uptake was depressed by 42% in arteries (P less than 0.05) and by 49% in veins (P less than 0.01) from hypertensive dogs, if incubated in the dog's own plasma. These results indicate that the activity of a ouabain-sensitive Na+-K+ pump may be depressed in vascular tissue from dogs with chronic one-kidney perinephritic hypertension. Because the Na+-K+ pump in vascular smooth muscle is probably electrogenic, such an abnormality, by partially depolarizing the muscle cell membrane, would help to account for the elevated vascular resistance found in these dogs.
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PMID:Depressed function of a ouabain-sensitive sodium-potassium pump in blood vessels from renal hypertensive dogs. 13 55

Guinea pig hindlimbs were unilaterally immobilized at resting length to evaluate histochemical, biochemical, and contractile properties of immobilized muscle. Contralateral limbs remained unrestrained. Four weeks later contractile properties were measured under chloral hydrate anesthesia. Average time-to-peak tension of the immobilized soleus was 30% less, whereas that of the gastrocnemius was not significantly changed relative to contralateral muscles. Immobilized soleus muscles acquired as much as 25% fibers with high alkaline myofibrillar adenosine triphosphatase activity; these fibers do not occur in the normal muscle. Neither the immobilized soleus nor gastrocnemius fatigued more quickly than their contralateral counterparts. In the immobilized gastrocnemius myofibrillar protein (mg/g muscle) decreased to 76% and maximum tetanic tension to 70% of contralateral values. However, tetanic tension per gram wet muscle weight or 100 mg myofibrillar protein was significantly greater in the immobilized gastrocnemius. No specific factor responsible for the increased tetanic tension could be identified.
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PMID:Properties of immobilized guinea pig hindlimb muscles. 13 3

Synaptosomes, or nerve-ending particles, were isolated from the cerebral cortices of young rats by homogenization, differential centrifugation, and density-gradient centrifugation. The sodium-potassium-activated adenosine triphosphatase enzyme system [(Na+ plus K+)-ATPase] of these particles is believed to represent in vitro the sodium-potassium pump of the nerve terminal. Suspensions of synpatosomes were equilibrated with air containing various concentrations of halothane and enflurane, as determined by gas chromatography. Clinical concentrations of the anesthetics had no effect on (Na+ plus K+)-ATPase activity. Fourteen per cent halothane and 14.8 per cent enflurane in the gas phase resulted in 12 and 10 per cent inhibition, respectively, of (Na+ plus K+)-ATPase activity. These data confirm that interference with active cation transport by inhibition of neuronal (Na+ plus K+)-ATPase is not related to the mechanism of halothane or enflurane anesthesia. (Key words: Anesthetics, volatile, halothane; Anesthetics, volatile, enflurane; Metabolism, enzymes, ATPase; Nerve, synaptosomal ATPase; Theories of anesthesia, ATPase.).
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PMID:The effects of halothane and enflurane on rat brain synaptosomal sodium-potassium-activated adenosine triphosphatase. 80 97

The mechanism of the anaesthetic effect of toluene on the central nervous system (CNS) was studied by using rat erythrocyte and synaptosome membranes as nerve cell models both in vitro and in vivo. The activities of the membrane-bound integral enzymes acetylcholinesterase (AChE), total adenosine triphosphatase (total ATPase) and magnesium-activated adenosine triphosphatase (Mg2+-ATPase) were determined. A short-term exposure to 2000 p.p.m. of toluene had an inhibitory effect on the enzyme activities studied. The degree of inhibition in erythrocyte membranes in vitro and in vivo, and in synaptosome membranes in vitro were in good correlation. In in vivo conditions, the synaptosome-bound enzymes were, however, significantly more inhibited by toluene, which indicates that membranes in vivo are even more vulnerable to the toxic effects of organic solvents than they are as isolated membranes in vitro. However, our results show that in vitro experiments can be used to predict the toxic nerve cell membrane effects of organic solvents. Toluene caused similar enzyme inhibitions both in neural cell membranes and in erythrocyte membranes. Thus, even peripheral non-excitable cell membranes, like erythrocytes, can be used as nerve cell membrane models in studies on the mechanism of the anaesthesia caused by solvents.
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PMID:The effect of in vitro and in vivo toluene exposure on rat erythrocyte and synaptosome membrane integral enzymes. 296 6

Infarction of the left ventricle was induced by ligation of the coronary artery in male Sprague-Dawley rats under ketamine-xylazine anesthesia. Three weeks after surgery, animals were assigned to a trained (n = 21; running at 20 m/min, 10% grade, 1 h/day, 5 days/wk) or nontrained group (n = 23) for an additional 8 wk. A third, sham-operated control group (n = 16) remained cage sedentary for 11 wk. Ventricular mass was greater in the trained and nontrained infarct groups [1,335 +/- 57.3 and 1,414 +/- 56.1 mg, respectively (mean +/- SE)] compared with the control group (1,155 +/- 50.9 mg) (P less than or equal to 0.05). The diameter of septal fibers was 13% greater in the trained and 17% greater in the nontrained infarct groups compared with control. The specific peak developed force and maximum rate of force development of left ventricular papillary muscle in vitro were 75 and 62% greater in both infarcted groups compared with the control group; these variables were unaffected by training. Myofibrillar adenosine triphosphatase activity of septum was 20% lower in both infarct groups compared with sham-operated animals. We conclude that exercise training did not alter the magnitude of morphological and physiological adaptations to infarction.
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PMID:Papillary mechanics and cardiac morphology of infarcted rat hearts after training. 362 52

1. Long-term electrical stimulation was given during 4 or 8 wk to the peroneal nerve of deafferented hindlimbs in hemispinalized adult cats. Four different stimulation patterns were compared: 100-Hz bursts covering 5% of daily time (F1), 10-Hz bursts covering 5% of daily time (S1), pattern S1 plus added 100-Hz bursts during 0.5% of daily time (S1F2), and, finally, only the latter 100-Hz bursts (F2), again during 0.5% of daily time. 2. During the course of chronic stimulation, frequent noninvasive measurements were made of the twitch of the ankle dorsiflexors. In a terminal acute experiment under general anesthesia, performed after 4 or 8 wk of treatment, measurements were made of isometric contractile properties (speed, force) for one of the stimulated peroneal muscles, m. peroneus longus (PerL). Thereafter, the PerL muscle was removed for further histochemical/histological analysis. 3. Findings from chronically stimulated PerL muscles were compared with three kinds of control PerL muscles: 1) those from the contralateral (control) hindlimb of chronically treated animals, 2) those from the operated side of animals that had been deafferented and hemispinalized but not subjected to chronic stimulation, 3) those from normal animals that had not been subjected to chronic treatment. With respect to the presently studied parameters, the three kinds of control muscles rendered very similar results. 4. All the presently used patterns of chronic stimulation made the PerL muscles slower with respect to twitch contraction time, half-relaxation time, and tension-frequency relation. Patterns covering 5-5.5% of daily time (F1, S1, S1F2) also caused an increase in the percentage of fibers classified as 'slow' (type I) on basis of their staining for myosin adenosine triphosphatase (ATPase). 5. Among patterns covering 5% of daily time, the change in ATPase histochemistry and the degree of physiological slowing was at least as pronounced after chronic stimulation at 100 Hz (F1) as after treatment at 10 Hz (S1). The slowing produced by pattern S1 was not more pronounced than that caused by this pattern (10 Hz) plus an equal number of pulses at 100 Hz (S1F2). 6. The slowing produced by the presently used patterns of chronic stimulation took place within the initial 2-3 wk. 7. Patterns F1 and S1 caused a decrease in maximum tetanic force as well as in mean fiber diameter.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of physiological amounts of high- and low-rate chronic stimulation on fast-twitch muscle of the cat hindlimb. I. Speed- and force-related properties. 365 84

Methanethiol (CH3SH) has been implicated in the pathogenesis of hepatic coma. Studies are presented to identify the possible biochemical basis of anesthesia-like effects of methanethiol and those features which distinguish such effects from common anesthetics and may represent the basis of its toxicity. CH3SH was found to stabilize erythrocyte membranes against hypotonic hemolysis at relatively low concentrations. At 37 degrees C the AH25 value for human erythrocyte antihemolysis was observed at a concentration of 0.34 mumol of CH3SH bound per mg of erythrocyte protein. Similar results were obtained with rat erythrocytes. This property of CH3SH is in common with other anesthetic agents. Anesthetic agents also inhibit the membrane-associated Na+,K+-adenosine triphosphatase (ATPase); however, for effective and nontoxic agents of this type the inhibition of ATPase activity is elicited at concentrations which are at least an order of magnitude higher than those which influence the membrane stability characterized by the antihemolysis effect (P. Seeman, Pharmacol. Rev. 24: 583-655, 1972). CH3SH was also found to inhibit the membrane Na+,K+-ATPase activity. The I25 value for the inhibition of human erythrocyte ATPase activity was obtained at CH3SH concentration of 0.12 mM which corresponded to 0.3 mumol of CH3SH bound per mg of erythrocyte membrane protein. Rat erythrocyte membrane ATPase was somewhat more sensitive to CH3SH. In all cases the binding of CH3SH to erythrocytes occurred primarily on the membrane. These results indicate that no differential exists with respect to the dose-response of these two activities associated with human erythrocyte membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of methanethiol on erythrocyte membrane stabilization and on Na+,K+-adenosine triphosphatase: relevance to hepatic coma. 631 65

Erythrocyte membrane adenosine triphosphatase activities were examined in twelve unipolar depressed patients receiving ECT. Eleven patients undergoing diagnostic cystoscopy served as controls for the acute effects of anaesthesia, and sixteen healthy subjects served as non-depressed controls. The unipolar depressed patients had a slight reduction in their (Na+ + K+)-ATPase activity but effective ECT treatment was not associated with any increase in this activity. This approach is unlikely to cast further light on the membrane phenomenology of depressive illness.
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PMID:Effect of electroconvulsive therapy on erythrocyte adenosine triphosphatase activity in depressive illness. 644 73

The in vivo anesthetic activity of monoketones in mice was examined in relation to their hydrophobicity and to the in vivo effects on Na+/K+ -adenosine triphosphatase (Na+/K+ -ATPase) activity and membrane fluidity. Anesthetic potency (AD50) of monoketones was determined; AD50 implys the dose required to anesthetize 50% of the animals from the treated group. The n-octanol/water partition coefficient (P) was used as an index of hydrophobicity. Membrane fluidity was determined by using 1,6-diphenyl-1,3,5-hexatriene (DPH) or 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH as fluorescence probes. Log (1/AD50) was the parabolic function of log P, log ((1/AD50) = -0.167(log P)2 + 0.698 log P - 1.365, and the log P that corresponds to the minimum AD50 was estimated to be 2.09. Brain synaptosomes were prepared from mice that were considered anesthetized with each of the 4 monoketones (1.5-fold AD50), methyl n-propyl, methyl n-amyl, methyl 3-methylhexyl and methyl n-octyl ketone. The Na+/K+ -ATPase activity was inhibited by methyl n-propyl ketone alone, membrane DPH fluidity was decreased by each of the 4 monoketones, and membrane TMA-DPH fluidity was decreased by methyl n-propylketone alone. These results suggest an involvement of the decreased DPH fluidity in monoketone-induced anesthesia.
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PMID:Anesthetic activity of monoketones in mice: relationship to hydrophobicity and in vivo effects on Na+/K+ -ATPase activity and membrane fluidity. 861 59

The objective of this study was to analyse the effects of isoflurane anesthesia (lasting for 15 or 60 min) and isoflurane anesthesia termination (after 1 or 24 h) on met-enkephalin (MENK) and leu-enkephalin (LENK) levels in discrete brain areas and spinal cord segments in rabbits. Moreover histochemical analysis of activities of succinate dehydrogenase, magnesium-dependent adenosine triphosphatase (Mg++ATP-ase) and acid phosphatase in the striatum and hypothalamus were carried out to evaluate the effects of isoflurane anesthesia on energetic, transport and catabolic processes. Throughout anesthesia (15 and 60 min) and after its termination (1 h) the LENK contents were increased in hypothalamus, hippocampus, mesencephalon and lumbar segment of spinal cord. Moreover, during isoflurane anesthesia and after its termination (1 h) MENK and LENK levels decreased in cervical segment and MENK content dropped in thoracic segment of spinal cord. Histochemical data indicated, that isoflurane enhanced energetic processes as well as exchange processes in neurocytes, glial cells, capillary walls and ependymal cells of the third ventricle. Measurements of acid phosphatase activity provided evidence of no signs of toxicity of isoflurane in the examined areas. The changes in enkephalin levels observed during the isoflurane anesthesia and after its termination depended on the type of examined neuropeptides, as well as on parts of the brain and spinal cord studied. The changes observed after isoflurane administration in enkephalinergic system are discussed with regard to our earlier experiments with halothane and enflurane.
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PMID:Influence of isoflurane on enkephalin levels and on some indicatory enzymes in the central nervous system of rabbits. 943 56


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