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

---

Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute starvation of adult rats resulted in a rise in the electroconvulsive threshold at 48 hours (P less than .10) and at 72 hours (P less than .01), but not at 24 hours. Biochemical correlates included (1) ketonemia and mild hypoglycemia in the blood; (2) a significant rise in the brain cytoplasmic phosphorylation potential and in the energy charge potential; (3) a shift in the brain cytoplasmic oxidation-reduction potential to a more oxidized state; (4) probable partial inhibitions in brain phosphofructokinase and pyruvate dehydrogenase; and (5) relatively small increases in brain sodium (4.1%), potassium (2.4%), and chloride (4.3%). No major differences were seen in brain water content or adenosine triphosphatase activity. The observed cerebral biochemical alterations are believed to be the consequence of increased ketone body utilization, although the precise relationship to the alteration in the electroconvulsive threshold remains unclear.
...
PMID:Starvation and seizures. Observation on the electroconvulsive threshold and cerebral metabolism of the starved adult rat. 12 78

A phytohemagglutinin extract is prepared from raw kidney beans (Phaseolus vulgaris) and incorporated at a level of 1% (dry matter) in the diet of young growing rats. Beside a decrease of feed intakes, the main effects of the experimental diet are the following : growth depression, decrease of dry matter and protein digestibility and hypoglycemia. Biological value, organs weight (liver, kidneys, spleen) did not change significantly. The hemagglutinin extract induces an inhibition of saccharase activity whereas (Na+-K+)-ATPase remains unchanged. Growth depressing effect may be due to an alteration of hydrolysis and absorption mechanisms at the level of brush border of enterocytes.
...
PMID:[Effects of a phytohemagglutinin extract on growth, nitrogen digestibility and the activity of invertase and (Na+-K+)-ATPase in the intestinal mucosa of the rat]. 23 10

Direct and indirect evidence suggests that Na+/K(+)-ATPase activity is reduced or insufficient to maintain ionic balances during and immediately after episodes of ischemia, hypoglycemia, epilepsy, and after administration of excitotoxins (glutamate agonists). Recent results show that inhibition of this enzyme results in neuronal death, and thus a hypothesis is proposed that a reduction and/or inhibition of this enzyme contributes to producing the central neuropathy found in the above disorders, and identifies potential mechanisms involved. While the extent of inhibition of Na+/K(+)-ATPase during ischemia, hypoglycemia and epilepsy may be insufficient to cause neuronal death by itself, unless the inhibition is severe and prolonged, there are a number of interactions which can lead to a potentiation of the neurotoxic actions of glutamate, a prime candidate for causing part of the damage following trauma. Presynaptically, inhibition of the Na+/K(+)-ATPase destroys the sodium gradient which drives the uptake of acidic amino acids and a number of other neurotransmitters. This results in both a block of reuptake and a stimulation of the release not only of glutamate but also of other neurotransmitters which modulate the neurotoxicity of glutamate. An exocytotic release of glutamate can also occur as inhibition of the enzyme causes depolarization of the membrane, but exocytosis is only possible when ATP levels are sufficiently high. Postsynaptically, the depolarization could alleviate the magnesium block of NMDA receptors, a major mechanism for glutamate-induced neurotoxicity, while massive depolarization results in seizure activity. With less severe inhibition, the retention of sodium results in osmotic swelling and possible cellular lysis. A build-up of intracellular calcium also occurs via voltage-gated calcium channels following depolarization and as a consequence of a failure of the sodium-calcium exchange system, maintained by the sodium gradient.
...
PMID:Inhibition of sodium-potassium-ATPase: a potentially ubiquitous mechanism contributing to central nervous system neuropathology. 166 97

Experiments on albino rats were made to investigate the activity of Na+, K(+)-ATPase and Mg(2+)-ATPase of fractions of microsomes and nerve endings, isolated from the cortex of the cerebral hemispheres, subcortical structures and medulla oblongata. The brain of healthy animals and that of rats in the state of insulin coma (40 units/kg of the hormone intramuscularly) were investigated at various periods after coma arrest with glucose. It has been assumed that an increase in the number of active molecules of Na+, K(+)-ATPase under the influence of structural changes of membranes in hypoglycemia cannot provide the electric activity of neurons in the absence of glycolytic ATP in neuroglycopenia.
...
PMID:[ATPase activity of rat brain microsomal and synaptosomal fractions in insulin hypoglycemia and its treatment with glucose]. 183 75

The role of extrarenal potassium homeostasis is well recognized as a major mechanism for the acute defense against the development of hyperkalemia. The purpose of this report is to examine whether or not the various mechanisms of extrarenal potassium regulation are intact in patients with end-stage renal disease (ESRD). The available data suggest that with the development of ESRD and the uremic syndrome there is impaired extrarenal potassium metabolism that is related to a defect in the Na,K-adenosine triphosphatase (ATPase). The responsiveness of uremic patients to the various effector systems that regulate extrarenal potassium handling is discussed. Insulin is well positioned to play an important role in the regulation of plasma potassium concentration in patients with impaired renal function. The role of basal insulin may be even more important than previously appreciated, since somatostatin infusion causes a much greater increase in the fasting plasma potassium in rats with renal failure than in controls. Furthermore, stimulation of endogenous insulin by oral glucose results in a greater intracellular translocation of potassium in uremic rats than in controls. Under at least two common physiologic circumstances, feeding and vigorous exercise, endogenous catecholamines might also act to defend against acute increments in extracellular potassium concentration. However, it is important to appreciate that the response to beta 2-adrenoreceptor-mediated internal potassium disposal is heterogeneous as judged by the variable responses to epinephrine infusion. Based on the evidence presented in this report, a regimen for the treatment of life-threatening hyperkalemia is outlined. Interpretation of the available data demonstrate that bicarbonate should not be relied on as the sole initial treatment for severe hyperkalemia, since the magnitude of the effect of bicarbonate on potassium is variable and may be delayed. The initial treatment for life-threatening hyperkalemia should always include insulin plus glucose, as the hypokalemic response to insulin is both prompt and predictable. Combined treatment with beta 2-agonists and insulin is also effective and may help prevent insulin-induced hypoglycemia.
...
PMID:Extrarenal potassium tolerance in chronic renal failure: implications for the treatment of acute hyperkalemia. 156 35

A 30-day ingestion of gamma-hexachlorocyclohexane (lindane) by carp (Cyprinus carpio) induced hypoglycemia without activation of two hepatic gluconeogenesis enzymes (fructose diphosphatase, EC 4.1.2.13, and glucose-6-phosphatase, EC 3.1.3.9) and hyponatremia and variations in muscle plasmic membrane-bound enzymes (especially cholinesterases, EC 3.1.1.7). After 109 days carps exhibited a decrease in natremia but no significant hypoglycemia. There was an activation of gluconeogenesis enzymes. Important changes were observed in the activities of muscle plasmic membrane enzymes (especially 5'-nucleotidase, EC 3.1.3.5, and ATPases, EC 3.6.1.3). Lindane, a lipophilic substance, especially disturbed the activity of membrane-bound enzymes enclosed in a phospholipid matrix.
...
PMID:Effect of gamma-hexachlorocyclohexane (lindane) on carp (Cyprinus carpio). II. Effects of chronic intoxication on blood, liver enzymes, and muscle plasmic membrane. 244 Jun 61

Severe insulin-induced hypoglycemia in rabbits reduces cerebrospinal fluid (CSF) formation, but not ventricular iodide clearance as measured by ventriculocisternal perfusion. This indicates that CSF production is ultimately glucose-dependent but that ventricular iodide clearance is not. The data suggest that severe hypoglycemia results in intracellular potassium loss within the brain and show that extracellular sodium replaces lost intracellular potassium. Hypoglycemia probably results in cellular adenosine triphosphate (ATP) reduction which affects membrane Na/K ATPase and the ability of the brain cell to maintain a potassium gradient. Potassium levels in the CSF also rise consequent to hypoglycemia. Homeostatic mechanisms that maintain a constant CSF potassium, therefore, are also affected by hypoglycemia.
...
PMID:The effect of severe hypoglycemia upon cerebrospinal fluid formation, ventricular iodide clearance, and brain electrolytes in rabbits. 625 65

The effects of acute insulin-induced hypoglycemia on the cerebral NMDA receptor in the newborn were examined by determining [3H]MK-801 binding as an index of NMDA receptor function in 6 control and 7 hypoglycemic piglets. In hypoglycemic animals, the glucose clamp technique with constant insulin infusion was used to maintain a blood glucose concentration of 1.2 mmol/l for 120 min before obtaining cerebral cortex for further analysis; controls received a saline infusion. Concentrations of glucose, lactate, ATP, and PCr were measured in cortex, and Na+,K(+)-ATPase activity was determined in a brain cell membrane preparation. [3H]MK-801 binding was evaluated by: (1) saturation binding assays over the range of 0.5-50 nM [3H]MK-801 in the presence of 100 microM glutamate and glycine; and (2) binding assays at 10 nM [3H]MK-801 in the presence of glutamate and/or glycine at 0, 10, or 100 microM. Blood and brain glucose concentrations were significantly lower in hypoglycemic animals than controls. There was no change in brain ATP with hypoglycemia, but PCr was decreased 80% compared to control (P < 0.05). Na+,K(+)-ATPase activity was 13% lower in hypoglycemic animals (P < 0.05). Based on saturation binding data, hypoglycemia had no effect on the number of functional receptors (Bmax), but the apparent affinity was significantly increased, as indicated by a decrease in the Kd (dissociation constant) from the control value of 8.1 +/- 1.6 nM to 5.5 +/- 2.1 nM (P < 0.05). Augmentation of [3H]MK-801 binding by glutamate and glycine alone or in combination was also significantly greater in the hypoglycemic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:The effect of acute hypoglycemia on the cerebral NMDA receptor in newborn piglets. 753 27

The effect of insulin induced hypoglycemia was studied on the activities of Acetylcholinesterase (AChE) which hydrolizes acetylcholine (ACh) and Na+, K(+)-ATPase, the enzymatic version of Na+,K(+)-pump from rat heart, liver and kidney. AChE activity was decreased significantly from two subcellular fractions of all the three tissues after 1,2 and 3 hours of insulin administration (5 units/100 gm body weight) Na+, K(+)-ATPase activity was decreased in liver and kidney, whereas, a significant increase in heart ATPase activity was observed. Blood glucose level was significantly lower than control values after 1, 2 and 3 hours of insulin injection, and the protein content from these tissues did not show any significant change under this physiological stress.
...
PMID:Effect of insulin induced hypoglycemia on acetylcholinesterase and Na+, K(+)-ATPase activity of rat heart, liver and kidney. 811 15

The activities of acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.1.1.7), responsible for hydrolysis of acetylcholine and Na+,K(+)-ATPase (Mg(2+)-dependent ATP phosphohydrolase, EC 3.6.1.3), which plays a crucial role in neurotransmission, were determined in four brain regions after 1, 2, and 3 h of insulin administration. Significant decrease in the acetylcholinesterase and Na+,K(+)-ATPase activities was observed in the soluble and total particulate fractions from cerebral hemispheres, cerebellum, brain stem, and diencephalon + basal ganglia after 1, 2, and 3 h of insulin-induced hypoglycemia. Blood glucose level decreased significantly after 1 h of insulin administration and remained at low level for 2 h thereafter, whereas, the protein content in different subcellular fractions from four brain regions did not show any significant change under this physiological stress.
...
PMID:Acetylcholinesterase and Na+,K(+)-ATPase activities in different regions of rat brain during insulin-induced hypoglycemia. 817 74


1 2 3 Next >>

---