Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

More than one type of voltage-gated calcium channel has been identified in muscle cells and neurons. Many specific organic and inorganic blockers of the conventional, slowly inactivating high threshold (L) calcium channel have been reported. No specific blockers of the low threshold (T) channel have been as yet identified. Amiloride, a potassium sparing diuretic, has now been shown to selectively block the low threshold calcium channel in mouse neuroblastoma and chick dorsal root ganglion neurons. The selective blockade of the T-type calcium channel will allow identification of this channel in different tissues and characterization of its specific physiological role.
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PMID:Amiloride selectively blocks the low threshold (T) calcium channel. 245 Dec 91

Previous reports from this laboratory have demonstrated that alpha 2-adrenergic receptors accelerate Na+/H+ exchange in NG108-15 neuroblastoma X glioma cells and evoke platelet secretion via a pathway involving Na+/H+ exchange. The present studies were designed to examine whether agents that interact with Na+/H+ antiporters also might influence alpha 2-adrenergic receptor-ligand interactions. We observed that Na+ decreases receptor affinity for the agonists epinephrine, norepinephrine, and UK14304 and slightly increases receptor affinity for the antagonists yohimbine and idazoxan in digitonin-solubilized preparations from porcine brain cortex. Increases in [H+] also decrease receptor affinity for agonists and cause either a slight increase or no change in receptor affinity for antagonists. Amiloride analogs accelerate the rate of [3H] yohimbine dissociation from digitonin-solubilized receptors with a relative effectiveness that parallels their ability to block Na+/H+ exchange in other systems. Interestingly, these modulatory effects of Na+,H+ and 5-amino-substituted analogs of amiloride are retained in homogeneous preparations of the alpha 2-adrenergic receptor, suggesting that the allosteric-binding sites for these agents are on the receptor-binding protein itself.
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PMID:Regulation of porcine brain alpha 2-adrenergic receptors by Na+,H+ and inhibitors of Na+/H+ exchange. 304 Jul 42

myo-Inositol uptake was investigated in a murine neuroblastoma clone (N1E-115) to determine the effect of altered Na+,K+-ATPase activity. The Na+ ionophore monensin, and veratridine, an alkaloid affecting voltage-dependent Na+ entry, increased acute 22Na+ uptake and 22Na+ efflux from pre-loaded cells, concomitant with enhanced myo-inositol uptake. This effect was also seen following insulin. Insulin-stimulated myo-inositol uptake was inhibited by amiloride, ouabain and pyrithiamine. Amiloride inhibition suggests that activation of Na+/H+ exchange preceding Na+,K+-ATPase activation is involved in insulin stimulation of myo-inositol uptake. Pyrithiamine inhibition is an indication of prior activation of the Na+,K+-ATPase alpha + catalytic subunit by insulin. The results provide evidence that insulin contributes to the maintenance of Na+,K+-ATPase in neuronal tissue.
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PMID:Acute changes in myo-inositol uptake and 22Na+ flux in murine neuroblastoma cells (N1E-115) following insulin. 330 13

The Na+ uptake into neuroblastoma x glioma hybrid cells was measured in Hepes-buffered EMEM containing 10% calf serum and 5 mM ouabain in the presence and absence of amiloride (1.0 mM). Amiloride was found to markedly inhibit net Na+ influx (by approximately 50%). Examination of the effect of amiloride on net Na+ influx in the absence of calf serum revealed that a significant amiloride-sensitive Na+ influx remains even under serum-deprived conditions, although the degree of amiloride inhibition (35%) is substantially lower than that found in the presence of serum. The amiloride-insensitive portion of Na+ influx was found to be independent of serum effects. Estimation of resting membrane potential was made by measurement of the steady state distribution of the lipophilic cation, TPP+, in the presence and absence of amiloride. A large, immediate increase in TPP+ uptake, indicative of a membrane hyperpolarization, was seen upon addition of amiloride. Determination of the effect of amiloride on resting membrane potential of serum-deprived cells showed that cells are hyperpolarized to a greater extent in the presence than in the absence of amiloride, and that serum exerts a depolarizing effect on the cells. Thus, serum-stimulation of Na+ influx results in a depolarization of resting membrane potential, while amiloride inhibition of Na+ influx causes a hyperpolarization. These data strongly suggest that NG108-15 cells possess an electrogenic Na+ influx pathway that is sensitive to amiloride inhibition and enhanced by serum.
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PMID:Membrane potential and sodium flux in neuroblastoma X glioma hybrid cells: effects of amiloride and serum. 717 41

The mechanism of cellular swelling induced by extra-cellular lactic acidosis and the effect of diuretics were studied using neuroblastoma-glioma hybrid (NG108-15) cells. The cells were incubated in one of three lactate concentrations (0, 15, or 30 mM), each of which was randomized to one of three pH groups (7.4, 6.2, or 5.0). Analysis of the swelling was measured using a Coulter counter technique. Cellular swelling was most prominent at pH 6.2 at all lactate levels. Cellular swelling was noted to be pH dependent but not lactate dependent. The addition of 1 mM amiloride completely blocked cellular swelling, suggesting that the main mechanism of neuronal cellular swelling induced by extracellular lactic acidosis was the activation of Na+/H+ exchange. Second, three dissimilar diuretic drugs were used for cellular swelling: amiloride (Na+/H+ exchange inhibitor), mannitol (osmotic diuretic), and bumetanide (loop diuretic). Amiloride and mannitol were found effective in reducing the lactic acidosis-induced cellular swelling. Furthermore, the combination of these drugs had additive effects. However, bumetanide was not effective. The results indicate that the direct inhibition of Na+/H+ exchange and/or removal of water from the cell by mannitol was effective against cellular swelling induced by the activation of Na+/H+ exchange in NG108-15 cells.
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PMID:Mechanism of cellular swelling induced by extracellular lactic acidosis in neuroblastoma-glioma hybrid (NG108-15) cells. 889 76