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)

The effects of gastric secretagogues, and other agents that modify H+,K(+)-ATPase activity and cell calcium concentration, on the rate of oxoglutarate oxidation were investigated in isolated gastric glands. Oxoglutarate was oxidized in a dose-dependent manner by gastric glands, with an apparent Km for oxoglutarate of 3.9 +/- 0.5 mM. Oxoglutarate progressively inhibited the rate of glucose oxidation. In the presence of 0.5 mM oxoglutarate plus 10 mM glucose, the latter substrate was preferentially oxidized and contributed most to oxygen uptake. With 10 mM oxoglutarate plus 10 mM glucose, the rate of glucose oxidation was greatly inhibited and oxoglutarate oxidation accounted for most of the oxygen consumption. Acid secretion (aminopyrine accumulation) was significantly increased by 0.1 mM histamine in glands oxidizing 10 mM oxoglutarate, although this stimulation was significantly lower than that observed in the presence of 0.5 mM oxoglutarate plus 10 mM glucose. Omeprazole, an inhibitor of the H+,K(+)-ATPase, significantly reduced the oxidation of oxoglutarate, whereas NH4+, an activator of the enzyme, stimulated the oxidation of a submaximal dose of oxoglutarate. Carbachol at 0.1 mM significantly increased the rate of oxidation of non-saturating concentrations of oxoglutarate. The calcium ionophore ionomycin at 10 microM produced a similar effect. Chelation of intracellular calcium by BAPTA AM caused a significant inhibition of oxoglutarate oxidation. The results provide further evidence that changes in the ATP:ADP ratio resulting from activation of the H+,K(+)-ATPase, and calcium ions are involved in the mechanisms of activation of oxidative metabolism in the parietal cell.
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PMID:Interactions between oxoglutarate oxidation and acid secretion in isolated rabbit gastric glands. 764 8

Recent studies of the smooth muscle contractile system indicate that Ca(2+)-dependent phosphorylation of the 20-kDa myosin light chains, modulation of phosphoprotein phosphatases, and phosphorylation of thin-filament proteins are all potential features of contractile system regulation. The thin-filament proteins caldesmon and calponin are known to inhibit actomyosin ATPase in vitro and actin sliding velocity in the in vitro motility assay. Inhibition of actomyosin ATPase is relieved by phosphorylation of caldesmon or calponin. The notion that caldesmon and calponin phosphorylation-dephosphorylation is important in the living smooth muscle cell was tested using canine tracheal smooth muscle strips labeled with 32P. We found that both caldesmon and calponin phosphorylation increased in response to stimulation with carbachol. Carbachol induced a biphasic increase in [Ca2+]i in canine tracheal smooth muscle, an early transient increase in myosin phosphorylation, which decayed to 0.4 mol Pi/mol light chain, and a rapid transient increase in tissue shortening velocity. Relative changes in caldesmon phosphorylation correlate best with force development and the [Ca2+]i transient, both of which follow a similar time course. Calponin phosphorylation appears to be a rapid transient event more similar to the transient increase in unloaded shortening velocity. Our results are consistent with a potential role for both caldesmon and calponin phosphorylation in regulating smooth muscle contraction.
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PMID:Caldesmon and calponin phosphorylation in regulation of smooth muscle contraction. 776 86

The activation of muscarinic receptors in N1E-115 neuroblastoma cells elicits a voltage-independent calcium current. The current turns on slowly, reaches its maximum value approximately 45 s after applying the agonist, is sustained as long as agonist is present, and recovers by one half in approximately 10 s after washing the agonist away. The current density is 0.11 +/- 0.08 pA/pF (mean +/- SD; n = 12). It is absent in zero-Ca++ saline and reduced by Mn++ and Ba++. The I(V) curve characterizing the current has an extrapolated reversal potential > +40 mV. The calcium current is observed in cells heavily loaded with BAPTA indicating that the calcium entry pathway is not directly gated by calcium. In fura-2 experiments, we find that muscarinic activation causes an elevation of intracellular Ca++ that is due to both intracellular calcium release and calcium influx. The component of the signal that requires external Ca++ has the same time course as the receptor operated calcium current. Calcium influx measured in this way elevates (Ca++)i by 89 +/- 41 nM (n = 7). Thapsigargin, an inhibitor of Ca++/ATPase associated with the endoplasmic reticulum (ER), activates a calcium current with similar properties. The current density is 0.22 +/- 0.20 pA/pF (n = 6). Thapsigargin activated current is reduced by Mn++ and Ba++ and increased by elevated external Ca++. Calcium influx activated by thapsigargin elevates (Ca++)i by 82 +/- 35 nM. The Ca++ currents due to agonist and due to thapsigargin do not sum, indicating that these procedures activate the same process. Carbachol and thapsigargin both cause calcium release from internal stores and the calcium current bears strong similarity to calcium-release-activated calcium currents in nonexcitable cells (Hoth, M., and R. Penner. 1993. Journal of Physiology. 465:359-386; Zweifach, A., and R. S. Lewis, 1993. Proceedings of the National Academy of Sciences, USA. 90:6295-6299).
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PMID:Calcium current activated by muscarinic receptors and thapsigargin in neuronal cells. 796 92

The mechanisms of cholinergic activation of carbohydrate metabolism were investigated in isolated rabbit gastric glands. Carbachol stimulated the rate of glucose oxidation in a dose-dependent fashion with a half-maximal effect occurring at approximately 9 microM. Atropine and omeprazole, but not cimetidine, completely blocked the stimulation induced by carbachol. Direct activation of the H(+)-K(+)-adenosinetriphosphatase by NH+4 caused a significant stimulation of glucose oxidation that was totally abolished by oligomycin and by the mitochondrial uncouplers dinitrophenol and carbonyl cyanide p-trifluoromethoxyphenylhydrazone. These latter agents did not abolish the stimulating effect of carbachol on glucose oxidation. Ionomycin increased the rate of glucose oxidation in a dose-dependent manner, and this effect was not blocked by oligomycin. The metabolic effect of ionomycin was reduced but not abolished by omeprazole. 1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester eliminated the carbachol-induced stimulation of glucose oxidation and partially inhibited the effect of NH+4. The mitochondrial enzymes pyruvate dehydrogenase and oxoglutarate dehydrogenase were activated by physiological concentrations of calcium in the isolated mitochondria. This effect was blocked by incubation with ruthenium red.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of cholinergic stimulation of glucose oxidation in isolated gastric glands. 807 23

We have studied the long-term effects of lithium on neuronal morphology and the functional expression of phospholipase C-coupled m3-muscarinic acetylcholine receptors (mAChRs) in cerebellar granule cells. There was a biphasic dose-dependent effect on cell morphology following treatment with lithium for 7 days. At low concentrations (< or = 2 mM), this drug elicited an increase in the number and thickness of connecting nerve fibers, and the size of neuronal aggregates. At high concentrations (5-10 mM), lithium induced a severe deterioration of cell morphology, which ultimately resulted in neuronal death. Carbachol-induced phosphoinositide (PI) turnover was similarly affected by lithium treatment with a significant potentiation at concentrations up to 2 mM and a marked inhibition at doses higher than 5 mM due to lithium-induced neurotoxicity. The biphasic effect on mAChR-mediated PI hydrolysis was associated with corresponding changes in the maximal extent of carbachol-induced inositol phosphate accumulation, and was accompanied by similar changes in [3H]N-methyl-scopolamine binding to mAChRs and the levels of mRNAs for m3-mAChR and c-Fos. The up-regulation of m3-mAChR mRNA induced by low concentrations of lithium was associated with a down-regulation of m2-mAChR mRNA and no change in either total RNA or beta-actin mRNA. Lithium's effects on m2- and m3-mAChR mRNAs were time-dependent, requiring a pretreatment time of > or = 3 days. The biphasic effect was also demonstrated by the binding of [3H]ouabain to Na+, K(+)-ATPase, which was shown to be a convenient method for quantifying viable neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term biphasic effects of lithium treatment on phospholipase C-coupled M3-muscarinic acetylcholine receptors in cultured cerebellar granule cells. 838 5

Glucose-induced insulin secretion is desensitized during long-term exposure of pancreatic islet beta-cells to elevated glucose levels. This study characterizes an in vitro model of glucose-induced desensitization in cultured isolated islets of the rat. Insulin secretion in desensitized islets cultured with 11 mM glucose for 4-7 days was progressively reduced compared with the normal freshly isolated (fresh) islets. When desensitized islets were returned to a basal concentration of glucose (5.5 mM) for up to 2 h, the glucose sensitivity of insulin secretion was restored to normal (recovered islets). Carbachol and L-arginine also reversed the effects of desensitization. However, basal insulin release was elevated in desensitized and recovered islets. Sodium-dependent myo-inositol uptake was reduced during desensitization by up to 49% within 4 days. myo-Inositol uptake was restored to normal in a time-dependent manner during recovery of islets at 5.5 mM glucose. The recovery of myo-inositol uptake paralleled that of insulin release. The apparent transport constant for myo-inositol uptake was significantly increased during desensitization, whereas the maximum uptake was not changed. myo-Inositol supplementation (35 or 250 microM) during islet culture did not alter myo-inositol uptake or insulin secretion in desensitized islets. Na(+)-K(+)-ATPase activity, but not 5'-nucleotidase activity, in desensitized islets was also inhibited by 65 and 47% when compared with fresh islet and recovered islet Na(+)-K(+)-ATPase activity, respectively. Thus, cultured islets represent an appropriate model to study biochemical parameters associated with the onset and reversibility of glucose desensitization of insulin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin secretion, myo-inositol transport, and Na(+)-K(+)-ATPase in glucose-desensitized rat islets. 839 25

Recently, it was reported that muscarinic-type cholinergic receptors coupled to the phosphoinositide messenger system are present in the rabbit inner medullary collecting duct and Madin-Darby canine kidney (MDCK) cells. The receptor density in MDCK cells is 50 times more than that in inner medullary collecting duct cells. To examine if muscarinic receptor activation influences Na-K-ATPase, the effects of a cholinergic agonist, carbachol, on Na-K-ATPase activity in MDCK cells were measured. Carbachol inhibited Na-K-ATPase activity in a time- and concentration-dependent manner. A maximum of approximately 80% of the enzyme activity was inhibited in 160 min with an EC50 of 5 microM carbachol. The inhibition of Na-K-ATPase activity was reversible; up to 80% of the enzyme activity was recovered within 4 h after carbachol was removed. The inhibitory effect of carbachol was blocked by a muscarinic antagonist atropine and by inhibitors of protein kinase C (PKC), 1-(5-isoquinolinesulfonyl)-2-methyl-piperazine HCl, and N-(2-(methylamino)ethyl)-5-isoquinoline sulfonamide HCl. Direct activators of PKC, phorbol 12-myristate 13-acetate, N(n-heptyl)-5-chloro-1-naphthalene sulfonamide, and phosphatidyl serine, also inhibited Na-K-ATPase activity in MDCK cells, and their effect was also blocked by PKC inhibitors. These results indicate that cholinergic agonists inhibit Na-K-ATPase activity in MDCK cells by the activation of PKC. It is concluded that the inhibition of Na-K-ATPase by PKC may, in part, be responsible for the natriuretic action of cholinergic agonists, which have been shown to stimulate phosphoinositide hydrolysis in renal collecting duct cells.
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PMID:Cholinergic inhibition of Na-K-ATPase via activation of protein kinase C in Madin-Darby canine kidney cells. 840 83

Single adult cardiac ventricular cells were prepared by collagenase perfusion of a rat heart. They were stimulated electrically in a perfusion chamber and their length changes were followed under a microscope. The motion was followed via a video camera and by a TV-line counting device and was recorded on-line by a personal computer. The program RECORD was used to calculate peak amplitude, base line drift and peak width at different peak heights allowing the determination of a number of variables of the cellular motion. The method was applied to drugs affecting the amplitude of contractions and the speed of relaxation. Results of beta-adrenergic stimulation, muscarinic inhibition and of the Ca(2+)-ATPase inhibitor cyclopiazonic acid (CPA) are shown. Besides its stimulatory effect on length, the beta-adrenergic agonist isoprenaline concentration-dependently shortened relaxation time. Carbachol reversed the increase in cellular shortening caused by isoprenaline in a concentration-dependent manner without fully reversing the shortened relaxation. CPA prolonged the return to diastole, presumably due to its inhibition of Ca(2+)-reuptake into the sarcoplasmatic reticulum.
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PMID:A computer program for motion analysis of single cardiac myocytes. 845 Apr 90

Na-K-ATPase is associated with a variety of membrane populations in lacrimal acinar cells. Acinus-like structures formed by rabbit acinar cells in primary culture were incubated with horseradish peroxidase (HRP) to label basolateral and endosomal membranes and then analyzed by electron microscopy cytochemistry with the 3-3'-diaminobenzidine reaction or by fractionation and measurement of marker catalytic activities or immunoreactivities. HRP adsorbed to basolateral membranes at 4 degrees C. Fractionation showed it associated with low-density membranes enriched in acid phosphatase and TGN38 but containing only minor amounts of Na-K-ATPase. Cells internalized HRP to cytoplasmic vesicles, Golgi structures, and lysosomes at 37 degrees C. The major endosomal compartment revealed by fractionation coincided with major peaks of Na-K-ATPase and Rab6 and secondary peaks of galactosyltransferase and gamma-adaptin. Carbachol (10 microM) increased lysosomal and Golgi labeling. Thus most of the Na-K-ATPase is located in the basolateral membrane-oriented endosomal system, concentrated in a compartment possibly related to the trans-Golgi network. Constitutive and stimulation-accelerated traffic to and from this compartment may serve several exocrine cell functions.
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PMID:Na-K-ATPase in lacrimal gland acinar cell endosomal system: correcting a case of mistaken identity. 894 53

We investigated Ca2+ handling in airway smooth muscle (SM) using fura 2 fluorescence, ion currents, and contractions as indexes of intracellular Ca2+ concentration ([Ca2+]i). Carbachol evoked a transient elevation of [Ca2+]i, the magnitude of which was smaller and the rate of decay faster at 37 degrees C, indicating that some temperature-sensitive mechanism contributed to recovery. Removal of external Na+ had no effect on agonist-evoked Ca2+ transients or contractions or on spontaneous Ca(2+)-dependent K+ currents. Cyclopiazonic acid, a selective inhibitor of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase, evoked a transient elevation of [Ca2+]i and contraction, markedly slowed recovery of the cholinergic Ca2+ transient, and depleted the SR. Sodium vanadate evoked a sustained elevation of [Ca2+]i and markedly slowed the decay of the cholinergic Ca2+ transient. We conclude that, in canine airway SM, 1) Na+/Ca2+ exchange makes at best only a minor contribution to Ca2+ homeostasis, 2) the SR Ca(2+)-ATPase compensates for spontaneous and agonist-triggered release of Ca2+, and 3) [Ca2+]i homeostasis involves some other extrusion pathway, likely the plasmalemmal Ca(2+)-ATPase.
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PMID:Regulation of [Ca2+]i in canine airway smooth muscle by Ca(2+)-ATPase and Na+/Ca2+ exchange mechanisms. 927 43


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