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)

1. The electrogenic effects of the Na(+)-K(+)-ATPase in thalamic neurones were investigated by means of intracellular and whole-cell patch-clamp recording techniques in rat medial geniculate body (MGB) maintained in vitro. 2. In twenty-six out of thirty-one neurones recorded intracellularly, application of the Na(+)-K+ pump inhibitor strophanthidin induced two different types of membrane depolarization: a small, reversible depolarization with a peak amplitude of 4 +/- 2.6 mV or a prolonged depolarization of large amplitude (48.6 +/- 9.0 mV) with or without a decrease in apparent membrane resistance. Blockade of glutamate receptors with kynurenic acid or 6-cyano-7-nitroquinoxaline-2,3-dione and (+/-)-2-amino-5-phosphonopentanoic acid did not prevent either type of pump response, but the large depolarization was not seen when the medium contained the sodium channel blocker TTX. 3. Whole-cell patch-clamp recording showed that the small membrane depolarization is mediated by an inward membrane current (39.00 +/- 5.70 pA) that exhibited a weak voltage dependence. An inward current of similar amplitude was also induced in MGB cells when the pipette solution contained nominally zero Na+ or when K+ was temporarily omitted from the extracellular medium. The large membrane depolarization or the corresponding membrane current was not observed in whole-cell conditions. 6. Transient inhibition of the electrogenic Na(+)-K(+)-ATPase consistently led to a change in the mode of synaptic transmission in MGB cells, during which the synaptically evoked burst response was either blocked or converted into a single spike discharge. 7. Taken together, these data suggest that blockade of the electrogenic pump produces a dual membrane effect in mammalian thalamic neurones: a small electrogenic membrane depolarization and a large depolarization response that can be prevented by artificially maintaining the transmembrane ionic gradients. The electrogenic activity of the Na(+)-K(+)-ATPase may play an important role in setting the mode of synaptic transmission in sensory thalamus.
...
PMID:The electrogenic effects of Na(+)-K(+)-ATPase in rat auditory thalamus. 926 17

We have examined whether arginine vasopressin (AVP) can induce a long-term modulation of transepithelial ion transport in addition to its well known short-term effect. In the RCCD1 rat cortical collecting duct cell line, an increase in both short-circuit current and 22Na transport was observed after several hours of 10(-8) M AVP treatment (a concentration above the in vivo physiological range). This delayed effect was partially prevented by apical addition of 10(-5) M amiloride and was blocked by 10(-6) M actinomycin D and 2 x 10(-6) M cycloheximide. The amounts of mRNA encoding the alpha1 (not beta1) subunit of Na+/K+-ATPase and the beta and gamma (not alpha) subunits of the amiloride-sensitive epithelial Na+ channel were significantly increased by AVP treatment. The increase in mRNA was blocked by actinomycin D, not by amiloride, suggesting a Na+-independent increase in the rate of transcription of these subunits. The translation rates of the alpha1 subunit of Na+/K+-ATPase and the beta and gamma subunits of the rat epithelial sodium channel increased significantly, whereas the translation rates of the other subunits remained unchanged. Finally, the number of Na+ channels present in the apical membrane of the cells increased, as demonstrated by enhanced specific [3H]phenamil binding.
...
PMID:Transcriptional regulation of sodium transport by vasopressin in renal cells. 940 70

The main mechanisms involved in the regulation of sodium transport by steroid hormones are briefly reviewed. The respective roles of the apical epithelial sodium channel, which is likely to be the limitant step of steroid-regulated transepithelial sodium transport, and Na,K-ATPase are described. Regulation of these ion transporting proteins by aldosterone and glucocorticoid hormones, probably via a two step mechanism (rapid activation of channels or pumps by unknown regulators, and modulation of the transcription/translation rate of these transporters), is discussed. The mechanisms of mineralocorticoid selectivity, that is, the integrated process allowing a specific action of aldosterone, in spite of high concentrations of glucocorticoids that crossbind with aldosterone to the mineralocorticoid receptor (MR), are explained, as is the role of the enzyme 11 beta-hydroxysteroid dehydrogenase and the differential interactions of MR with steroid ligands and hormone responsive elements of DNA. Finally, synergism between aldosterone and antidiuretic hormone for the stimulation of sodium transport is evoked.
...
PMID:Regulation of sodium transport by steroid hormones. 955 32

Rats exposed to 85% O2 for 5-7 days develop tolerance to otherwise lethal hyperoxia (100% O2). The rate of alveolar fluid clearance increases during adaptation to hyperoxia, due in part to increased alveolar epithelial sodium channel activity. In these studies, we have investigated molecular mechanisms leading to increased lung Na+,K(+)-ATPase activity in hyperoxia. We exposed adult rats to 85% O2 (sublethal hyperoxia) for 7 days, followed by 2, 3, or 4 days in 100% O2. Steady-state levels of the Na+,K(+)-ATPase alpha 1 and beta 1 subunit mRNAs increased in whole lung tissue during hyperoxia exposures. Stability of the Na+,K(+)-ATPase alpha 1 and beta 1 subunit mRNA messages in whole lung RNA did not change significantly. Thus, lung Na+,K(+)-ATPase gene expression in sublethal hyperoxia appears to be regulated in part at the transcriptional level. Alveolar epithelial type II (ATII) cell Na+,K(+)-ATPase alpha 1 and beta 1 subunit proteins, measured by quantitative immunofluorescence, increased significantly after sublethal hyperoxia and 100% O2 exposures. Increases in lung fluid clearance after sublethal hyperoxia are associated with increased ATII cell Na+,K(+)-ATPase protein and whole lung Na+,K(+)-ATPase mRNA expression, which correspond to previously described increases in epithelial sodium channel expression under these conditions.
...
PMID:Modulation of rat lung Na+,K(+)-ATPase gene expression by hyperoxia. 955 75

Significant progress have been made in understanding the mechanisms of alveolar fluid clearance at the time of birth and the transition from placental oxygenation to air breathing. During fetal life, the mammalian lung is a fluid filled secretory organ that fills no respiratory function. Its potential air spaces are filled with fluid that is actively secreted in response to an osmotic force generated by Cl(-)-secretion and the fluid-filled lung is necessary for a proper development of the air-breathing lung. As term approaches, net Cl(-)-secretion decreases, which is accompanied by a decreased secretion rate of the fluid into the air spaces. Concomitantly with the decreased Cl(-)-secretion, the alveolar epithelium begins to absorb Na+ to prepare for fluid absorption and the air breathing life. The causes for the decreased Cl(-)-secretion and the beginning of the Na+ absorption are not clear. Alterations in the hormonal milieu of the lung as well as changes in plasma stress hormone levels have been suggested to play roles. The switch from a placental oxygenation to pulmonary oxygenation requires that the fluid in the air spaces be rapidly removed from the lung lumen. Recent studies have demonstrated that removal of the alveolar fluid at birth is regulated via endogenous plasma epinephrine in the newborn. Molecular, cellular, and whole animal in vivo studies have demonstrated that fluid absorption at birth is related to expression and function of the epithelial sodium channel (ENaC). Several different in vivo and in vitro preparations have been used to investigate the mechanisms of alveolar fluid transport, primarily in adult lungs and have demonstrated that alveolar fluid absorption is driven by active Na+ transport. Both catecholamine-dependent and -independent regulatory mechanisms have been identified, probably acting on ENaC and other apical sodium channels and/or the basolaterally located Na+, K(+)-ATPase. Future studies are needed to integrate new insights to the molecular mechanisms behind fluid clearance with their function in both normal and pathological lungs.
...
PMID:Salt and water transport across the alveolar epithelium in the developing lung: correlations between function and recent molecular biology advances (Review). 985 47

Morphine was shown to decrease in a dose-dependent manner the effective charge transfer in tetrodotoxin-resistant (TTXr) sodium channel activation system in short-term cultured dorsal root ganglion cells. Morphine seems to interact with opioid receptors because of total block of the binding by naloxone and naltrexone. Neither activating, nor inhibiting G-protein agents exerted any effect on this process. The morphine signal was blocked by extracellular application of 2 x 10(-4) M ouabain. The findings suggest existence of sodium signalling pathway involving receptors, Na+, K(+)-ATPase and the TTXr sodium channels.
...
PMID:[Morphine decreases the voltage sensitivity of the slow sodium channels]. 1038 79

The role of cell type-specific Na+,K+-ATPase isozymes in function-related glucose metabolism was studied using differentiated rat brain cell aggregate cultures. In mixed neuron-glia cultures, glucose utilization, determined by measuring the rate of radiolabeled 2-deoxyglucose accumulation, was markedly stimulated by the voltage-dependent sodium channel agonist veratridine (0.75 micromol/L), as well as by glutamate (100 micromol/L) and the ionotropic glutamate receptor agonist N-methyl-D-aspartate (NMDA) (10 micromol/L). Significant stimulation also was elicited by elevated extracellular potassium (12 mmol/L KCl), which was even more pronounced at 30 mmol/L KCl. In neuron-enriched cultures, a similar stimulation of glucose utilization was obtained with veratridine, specific ionotropic glutamate receptor agonists, and 30 mmol/L but not 12 mmol/L KCl. The effects of veratridine, glutamate, and NMDA were blocked by specific antagonists (tetrodotoxin, CNQX, or MK801, respectively). Low concentrations of ouabain (10(-6) mol/L) prevented stimulation by the depolarizing agents but reduced only partially the response to 12 mmol/L KCl. Together with previous data showing cell type-specific expression of Na+,K+-ATPase subunit isoforms in these cultures, the current results support the view that distinct isoforms of Na+,K+-ATPase regulate glucose utilization in neurons in response to membrane depolarization, and in glial cells in response to elevated extracellular potassium.
...
PMID:Separate neuronal and glial Na+,K+-ATPase isoforms regulate glucose utilization in response to membrane depolarization and elevated extracellular potassium. 1047 57

In the constant flow perfused rat hind limb, norepinephrine (NE) evoked increases in oxygen uptake (VO2) and lactate efflux (LE) were inhibited by the cardiac glycoside ouabain (1 mM), without interrupting the NE-mediated vasoconstriction. The membrane labilizer veratridine, previously shown to increase VO2 and LE, without increasing perfusion pressure, was also shown to be inhibited by the cardiac glycoside ouabain, as well as by the ouabain analogues digitoxin and digoxin. The stimulatory actions of veratridine on VO2 were inhibitable by low doses of the specific sodium channel blocker tetrodotoxin (TTX), while NE effects were unaffected, suggesting that NE may be acting via a TTX-insensitive sodium channel. It is concluded that agents such as NE (a vasoconstrictor) or veratridine (a membrane labilizer), which stimulate VO2 in the perfused rat hind limb, do so by increasing Na+ influx. The observed increases in oxygen consumption and LE are due to Na+-K+ ATPase activity to pump Na+ out of the cell at the expense of ATP turnover. Energy dissipation due to Na+ cycling may be a form of facultative thermogenesis attributable to NE that can be stimulated by membrane labilizers such as veratridine in the constant flow perfused rat hind limb.
...
PMID:Na+ channel and Na+-K+ ATPase involvement in norepinephrine- and veratridine-stimulated metabolism in perfused rat hind limb. 1053 84

Intratracheal infection of mice with adenovirus is associated with subsequent pulmonary inflammation and edema. Water movement through the air space-capillary barrier in the distal lung is facilitated by aquaporins (AQPs). To investigate the possibility that distal lung AQPs undergo altered regulation under conditions of aberrant fluid handling in the lung, we analyzed messenger RNA (mRNA) and protein expression of AQPs 1 and 5 in the lungs of mice 7 and 14 d after infection with adenovirus. Here, we demonstrate that AQP1 and AQP5 show decreased expression following adenoviral infection. Northern blot analysis showed significantly decreased mRNA levels of AQP1, which is expressed in the capillary endothelium, and AQP5, which is expressed in alveolar epithelium, in the lungs of mice both 7 and 14 d after infection. Immunoblotting studies demonstrated significantly reduced levels of AQP1 and AQP5 protein after infection as well. In addition, mRNA expression of the alpha subunit of the epithelial sodium channel was reduced in the lungs of mice 7 and 14 d after adenoviral infection. In contrast, mRNA expression of the alpha1 subunit of the Na,K-adenosine triphosphatase in the lung was unaltered. Immunohistochemical analysis demonstrated that the decreases in AQP1 and AQP5 expression were not localized to regions of overt inflammation but were found throughout the lung. Thus, this study provides the first report of AQP gene regulation in an in vivo model of pulmonary inflammation and edema. Decreased AQP1 and AQP5 levels during adenoviral infection suggest a role for AQP1 and AQP5 in the abnormal fluid fluxes detected during pulmonary inflammation.
...
PMID:Decreased expression of aquaporin (AQP)1 and AQP5 in mouse lung after acute viral infection. 1061 63

Pyrethrins are widely used insecticides in both agriculture and households. In many commercial formulations piperonyl butoxide (PBO) is used with pyrethrins. PBO is a well-known synergist of pyrethrins, used to intensify their effects. One of the cellular targets of pyrethrins is the sodium channel in the membrane. In the present study, the activity of the membrane-bound integral protein ATPase was studied as a biomarker for the membrane effects of pyrethrin and PBO. Cerebral synaptosomes of rat brain were used in the study. The isolation of synaptosomes was performed with the Percoll gradient method. Both total ATPase and Mg2+ activated ATPase were studied by determining inorganic phosphate. Exposure to 0.1-1000 microM of pyrethrin and to 0.4-4000 microM of PBO decreased ATPase activity dose-dependently. The most efficient mixture was the one consisting of one part of pyrethrin and four parts of PBO. The activity of total ATPase decreased 15% in concentrations of 0.1-10 microM pyrethrin, and a 50% decrease was found at 100 microM pyrethrin. The mixture of pyrethrin and PBO caused a 15-60% decrease in the total ATPase activity at 0.1-10 microM pyrethrin and 0.4-40 microM PBO. A 85% decrease was found after exposure to the mixture of 100 microM pyrethrin and 400 microM PBO. PBO alone had no effect at 0.4-40 microM concentrations, but a marked effect was seen at over 40 microM concentrations. The results indicate that PBO is an effective synergist of pyrethrin and that it is very toxic in high concentrations. The results also confirm that neuronal sodium homeostasis is one target of the neurotoxic effect of pyrethroid compounds.
...
PMID:Piperonyl butoxide potentiates the synaptosome ATPase inhibiting effect of pyrethrin. 1066 20


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---