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)

We studied the effect of cardiac ischemia on sarcolemmal enzymes, Na+-Ca2+ exchange, Ca2+ binding, and Ca2+ efflux in the newborn and adult rabbit. Rabbit ventricle was made ischemic by incubation in hypoxic, glucose-free Tyrode solution at 37 degrees C for 60-120 min. Ischemia inhibited Na+-K+-ATPase and K+-p-nitrophenylphosphatase (PNPPase) activity in the adult myocardium more than in the newborn. In the oxygenated (control) hearts, Na+-Ca2+-exchange activity in the newborn sarcolemma [Michaelis constant (Km) 18 microM; maximum velocity (Vmax) 33] was similar to that in the adult (Km = 16 microM, Vmax = 32). After 60 min ischemia, however, Na+-Ca2+ exchange in the newborn (Km = 16 microM, Vmax = 18) was inhibited less than in the adult (Km = 25 microM, Vmax = 18). In the two age groups, Ca2+ binding and efflux rate were not increased after ischemia, which suggested that Ca2+ permeability did not increase during ischemia. In conclusion, ischemia inhibited sarcolemmal enzymes and Na+-Ca2+ exchange in the newborn less than in the adult, and this lesser inhibition might contribute to or be caused by the greater tolerance of the newborn heart to ischemia.
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PMID:Effect of ischemia on sarcolemmal Na+-Ca2+ exchange in neonatal hearts. 254 10

High affinity [3H]ouabain binding was examined in the hippocampal CA1 region and frontal cortex of rats subjected to 5 min complete cerebral ischemia in a clinical death model, and to subsequent resuscitation. A decrease of Bmax directly after ischemia and its further gradual decrease during 120 min of reperfusion were noted in the ischemia-vulnerable CA1 region, whereas no change of Bmax was observed in frontal cortex. The apparent Kd constant showed insignificant fluctuations in either of the two brain regions. Since ouabain binds with high affinity to the neuronal (alpha +)-form of Na+/K+-ATPase, the results indicate a rapid enzyme loss in CA1 neurons. The high affinity ouabain binding test proved to be a sensitive detector of premorphological changes in nerve cell membranes in ischemia.
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PMID:Rapid decrease of high affinity ouabain binding sites in hippocampal CA1 region following short-term global cerebral ischemia in rat. 254 99

1) The primary receptor mechanism of catecholamine-induced myocardial potassium uptake is beta 1-adrenoceptor stimulation. Thus, K+ uptake seems to be a general effect of beta-adrenergic stimulation, dominated by beta 1-receptors in heart and by beta 2-receptors in skeletal muscle according to subtype preponderance in either tissue. In the myocardium there is also an effect of alpha 1-adrenoceptor stimulation which causes a significantly smaller uptake and requires higher catecholamine concentrations. 2) Both humoral and nervous adrenergic stimulation of the heart induce a significant potassium uptake which transiently reduces coronary sinus K+ concentration. It is likely that these changes affect cardiac functioning in vivo. During intense endogenous sympathetic activity and by high dose pharmacological interventions, the magnitude of change in coronary sinus concentration suggests that the reduction in extracellular K+ within the myocardium could be up to 1 mM. Under vulnerable conditions like hypokalemia and localized ischemia such changes might contribute to the risk for malignant arrhythmias. 3) Presumably net myocardial K+ accumulation is accompanied by a reciprocal reduction of intracellular Na+ concentration, which tends to reduce myocardial contractility and contribute to impaired cardiac function after a period of strong adrenergic stimulation. In vivo the negative inotropic effect could not be detected as long as catecholamines were supplied, but it occurred after stimulation was stopped. 4) In the intact beating heart beta-adrenergic stimulation increases Na,K-pumping 2.5 fold, from 15% of the maximum possible pump rate in control to 40% of maximum at high inotropy. These findings imply the presence of a substantial spare Na,K-pump capacity of the non-ischemic myocardium, even during intense sympathetic activity. Comparison of changes in pump rate and accumulated ionic shifts indicates that catecholamine-induced stimulation of Na,K-ATPase might be due to increased sensitivity for intracellular sodium.
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PMID:Myocardial potassium balance during adrenergic stimulation. 254 22

Ischemia gives rise to severe energy depletion and imbalance of Ca2+ homeostasis. This condition leads to activation of phospholipases A2, A1 and to attenuation of ATP dependent reacylation. As a result, free fatty acid (FFA) especially arachidonic acid accumulates. Phenytoin has been reported to blockade the various Ca2+ channels. In this study, we could investigate the effect of phenytoin on the liberation of FFA, energy metabolites, various nucleotides metabolism, Na+, K+-ATPase activity, and water and electrolyte contents in the ischemic brain. Inhibitory effects of phenytoin against FFA accumulation in the ischemia, and increase of parietal cortex water content in the recirculation were brought about. In addition, Na+,K+-ATPase activity in the ischemia was accelerated by phenytoin. Phenytoin may reduce intracellular Ca2+ by blocking the Ca2+ channel into the cytoplasma, or by activation of Na+-Ca2+ exchange transport system following the acceleration of Na+,K+-ATPase activity. Another conceivable way for this acceleration of Na+,K+-ATPase may be derived from the preservation of the energy state, protein metabolism, and lipid metabolism.
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PMID:[A study on the protective mechanism of phenytoin in transient global ischemia]. 255 Aug 30

A viable suspension of proximal tubules that had sustained an in vivo ischemic injury was harvested, and cellular integrity and viability were determined. The histopathological appearance of this preparation has characteristic features of an ischemic injury and ATP levels were comparable to those observed with nuclear magnetic resonance spectroscopy in vivo. Sprague-Dawley rats were subjected to 45 min of bilateral renal artery ischemia and the kidneys were allowed to reperfuse for either 15 min, 2 h, or 24 h before the harvest of the proximal tubule suspension. There was a decrease in base-line oxygen consumption from 34 +/- 0.8 nmol O2.min-1.mg protein-1 to 22 +/- 0.6 at 15 min of reflow. This decline in oxygen consumption persisted during the first 2 h of reflow and returned to control levels by 24 h. Residual respiration in the presence of ouabain was similar at all reflow intervals suggesting that the decrease in basal O2 consumption was related to decreased Na+-K+-ATPase in situ. In contrast, there was no significant difference in Na+-K+-ATPase activity when determined chemically under Vmax conditions in all experimental groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic alterations in proximal tubule suspensions obtained from ischemic kidneys. 255 Nov 86

In proximal tubular cells ischemia is known to result in the redistribution of apical and basolateral domain-specific lipids and proteins into the alternate surface membrane domain. Since tight junctions are required for the maintenance of surface membrane polarity, the effect of ischemia on tight junction functional integrity was investigated. In vivo microperfusion of early loops of proximal tubules with ruthenium red (0.2%) in glutaraldehyde (2%) was used to gain selective access to and outline the apical surface membrane. Under control situations ruthenium red penetrated less than 10% of the tight junctions. After 5, 15, and 30 min of ischemia, however, there was a successive stepwise increase in tight junction penetration by ruthenium red to 29, 50, and 62%, respectively. This was associated with the rapid duration-dependent redistribution of basolateral membrane domain-specific lipids and NaK-ATPase into the apical membrane domain. Taken together, these data indicate that during ischemia proximal tubule tight junctions open, which in turn leads to the lateral intramembranous diffusion of membrane components into the alternate surface membrane domain.
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PMID:Ischemia-induced loss of epithelial polarity. Role of the tight junction. 255 26

m-Nisoldipine 4, 8, 16 nmol/L, nisoldipine 1, 4 nmol/L and nifedipine 4, 8, 16, 50 nmol/L enhanced the recoveries of functional parameters of working rabbit hearts after ischemia-reperfusion, as well as prevented the development of contracture and the release of CPK from the reperfused hearts. m-Nisoldipine 8 nmol/L, nisoldipine 1 nmol/L and nifedipine 8 nmol/L attenuated the reduction of myocardial Na+-K+-ATPase and 5'-nucleotidase activity induced by ischemia-reperfusion. The breakdown of membrane phospholipids and elevation of the myocardial Ca2+-ATPase activity and the free fatty acids level were also prevented.
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PMID:[Protective effects of m-nisoldipine and nisoldipine on myocardial damage in working rabbit hearts after ischemia-reperfusion]. 255 66

The total time-controlled ischemia (up to 45 min) was studied for its effect on the Na,K-ATPase activity, content of nonesterified fatty acids (NEFA) and intensity of lipid peroxidation (LP) in sarcolemmal (SL) preparations and soluble fractions (SF) from the rat and guinea-pig left ventricles. A strong correlation between Na, K-ATPase inhibition and NEFA accumulation was revealed in the SF. On the contrary, changes in the NEFA content and LP level both in SL and SF did not correlate with a decrease in the enzymic activity. Pretreatment with albumin (0.5 mg/ml) induced equally small increase both in the control and in the ischemic SL preparations. It is suggested that the Na,K-ATPase activity during a short period of myocardial ischemia (up to 45 min) may be due to the NEFA accumulation in the cytosolic and/or extracellular space, but not in SL.
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PMID:[Na,K-ATPase activity in the myocardial sarcolemma in ischemia]. 255 47

The main purpose of our study is to investigate the possible protective effects of Fructose 1-6 diphosphate (FDP) and Danshen (Salvia Miltiozzhiza Bunze) on renal cortical Na-K-ATPase activity after renal ischemia and gentamicin nephrotoxicity. An 18.6% reduction in renal cortical Na-K-ATPase activity was shown after 30 min of renal pedicle clamping and 60 min of reflow, and a 32.5% reduction after 90 min of single injection of 100 mg/kg gentamicin. Light and electronic microscopy revealed no significant morphologic changes in both groups in the experiment. 4g/kg FDP and 18g/kg Danshen were infused 60 min after reflow in the ischemic group, 90 min after injection of gentamicin in the gentamicin-treated group and 90 min in the sham-operated group separately. The enzyme activity in the FDP-treated groups was found to be higher than that in the control kidneys while in the Danshen-treated groups no significant difference could be found. Our study showed that FDP and Danshen could prevent the decline of renal cortical Na-K-ATPase activity induced by ischemia and gentamicin. FDP could increase this enzyme activity while Danshen showed no such direct effect.
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PMID:Effects of FDP and Danshen on renal cortical Na-K-ATPase activity in rats after treatment with renal ischemia and gentamicin. 256 Sep 55

The calmodulin content in cardiomyocyte cytosol of hypoxic myocardium is increased compared to normal level. This is unaccompanied by differences in the stimulating effect of calmodulin on Ca2+ transport in sarcoplasmic reticulum (SR) of ischemic heart. The decrease of the endogenous cAMP-dependent protein kinase activity in ischemia is associated with the lowered resistance to trypsinolysis of Ca2+ transport in SR (trypsin/microsomal protein ratio is 1:10) with simultaneous Ca-ATPase activation. In the presence of exogenous protein kinase and cAMP the protective effect of phosphorylation on Ca2+ transport in SR vesicles of hypoxic cardiomyocytes treated with trypsin for 10 min reaches the same level as in intact heart.
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PMID:[cAMP, calmodulin-dependent stimulation and stability to proteolysis of Ca 2+ transport in the heart sarcoplasmic reticulum]. 256 Dec 65


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