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 interaction of various hormones and regucalcin on (Ca(2+)-Mg2+)-ATPase activity in rat liver plasma membranes was investigated. The presence of epinephrine (10(-6)-10(-4) M), phenylephrine (10(-6)-10(-4) M), and insulin (10(-8)-10(-7) M) in the reaction mixture produced a significant increase in (Ca(2+)-Mg7+)-ATPase activity, while the enzyme activity was decreased significantly by calcitonin (3 x 10(-8)-3 x 10(-6) M). These hormonal effects, except for calcitonin, were clearly inhibited by the presence of vanadate (10(-4) M) which can inhibit the Ca(2+)-dependent phosphorylation of enzyme. Meanwhile, regucalcin (0.25 and 0.50 microM), isolated from rat liver cytosol, elevated significantly (Ca(2+)-Mg2+)-ATPase activity in the plasma membranes, although this elevation was not inhibited by vanadate (10(-4) M). The epinephrine (10(-5) M) or phenylephrine (10(-4) M)-induced increase in (Ca(2+)-Mg2+)-ATPase activity was disappeared in the presence of regucalcin; in this case the effect of regucalcin was also weakened. However, the inhibitory effect of calcitonin (3 x 10(-6) M) was not weakened by the presence of regucalcin (0.5 microM). Moreover, GTP (10(-5) and 10(-4) M)-induced increase in (Ca(2+)-Mg2+)-ATPase activity was not seen in the presence of regucalcin (0.25 microM). The present finding suggests that the activating mechanism of regucalcin on (Ca(2+)-Mg2+)-ATPase is not involved on GTP-binding protein which modulates the receptor-mediated hormonal effect in rat liver plasma membranes.
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PMID:Regucalcin modulates hormonal effect on (Ca(2+)-Mg2+)-ATPase activity in rat liver plasma membranes. 828 72

Antidiuretic hormone and parathyroid hormone (PTH) inhibit HCO3- absorption by the rat medullary thick ascending limb (MTAL). Studies were performed on rat MTAL tubule suspension to specify the H(+)-HCO3- membrane transporters affected by these hormones and the implicated intracellular second messengers. Arginine vasopressin (AVP) and PTH stimulated cell adenosine 3',5'-cyclic monophosphate (cAMP) production with a relative rank order potency of AVP > rat PTH-(1-34) > bovine PTH-(1-84). Significant cell acidification in HCO3- -CO2-free medium, monitored in 2'7'-bis(carboxyethyl)-5(6')-carboxyfluorescein-loaded cells, was caused by 0.1 nM AVP, 1 nM rat PTH-(1-34), but not by < 100 nM bovine PTH-(1-84), as well as by 10(-4) M 8-bromo-cAMP and 2 x 10(-5) M forskolin; 10 nM AVP or rat PTH-(1-34) did not alter the intracellular pH when Na+/H+ antiport was inhibited by 2 mM amiloride. Prostaglandin E2 (PGE2, 10(-6) M), which inhibited AVP-stimulated cell cAMP production, reduced by 35% the cell acidification response to 10 nM AVP. AVP and 8-bromo-cAMP inhibited Na+/H+ antiport-dependent cell pH recovery from intracellular acidification, which was explained by a decrease in the Vmax of the antiporter. AVP did not directly affect K(+)-HCO3- cotransport and plasma membrane H(+)-ATPase of rat MTAL cells. Cytosolic calcium ([Ca2+]i), monitored in fura-2-loaded cells, was unaffected by up to 1 nM AVP, 100 nM PTH, glucagon, calcitonin, and oxytocin, and 1 microM PGE2; however, 100 nM AVP, but not 1-desamino-8-D-AVP (dDAVP), caused a peak increase in [Ca2+]i, even in the absence of extracellular Ca2+, and stimulated cell accumulation of [3H]inositol phosphates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:cAMP-dependent control of Na+/H+ antiport by AVP, PTH, and PGE2 in rat medullary thick ascending limb cells. 838 52

The expression of laminin, Na+, K(+)-ATPase, carbonic anhydrase (CA) isoenzymes and calcitonin gene-related peptide (CGRP) in the human fetal vestibular ganglia was studied by immuno-histochemistry. In the 12-week-old fetus, the cell surface of the vestibular ganglion cells was positive for laminin. In the 14-week-old fetus, a few vestibular ganglion cells were positive for CA II. In the 15-week-old fetus, the cell surface of the vestibular ganglion cells and the nerve fibers were strongly labelled with laminin. CGRP positive nerve fibers were found in the ganglia. In the 16-week-old fetus, some ganglion cells were labelled with Na+, K(+)-ATPase. CA II stained the vestibular nerve fibers as well as the vestibular ganglion cells. The results suggest that these substances may be used as histological markers of maturation and innervation of the human vestibular ganglion cells.
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PMID:The expression of maturation factors in the vestibular ganglia in the human fetus. 838 67

Past knowledge and the recent developments on the formation, activation and mode of action of osteoclasts, with particular reference to the regulation of each individual step, have been reviewed. The following conclusions of consensus have emerged. 1. The resorption of bone is the result of successive steps that can be regulated individually. 2. Osteoclast progenitors are formed in bone marrow. This is followed by their vascular dissemination and the generation of resting preosteoclasts and osteoclasts in bone. 3. The exact pathways of differentiation of the osteoclast progenators to mature osteoclasts are debatable, but there is clear evidence that stromal cells support osteoclast generation. 4. Osteoclasts are activated following contact with mineralized bone. This appears to be controlled by osteoblasts that expose mineral to osteoclasts and/or release a factor that activates these cells. 5. Activated osteoclasts dissolve the bone mineral and digest the organic matter of bone by the action of agents secreted in the segregated microcompartments underlying their ruffled borders. The mineral is solubilized by protons generated from CO2 by carbonic anhydrase and secreted by an ATP-driven vacuolar H(+)-K(+)-ATPase located at the ruffled border. The organic matrix of the bone is removed by acid proteinases, particularly cysteine-proteinases that are secreted together with other lysosomal enzymes in the acid environment of the resorption zone. 6. Osteoclastic bone resorption is directly regulated by a polypeptide hormone, calcitonin (CT), and locally, by ionized calcium (Ca2+) generated as a result of osteoclastic bone resorption. 7. There is new evidence that osteoclast activity may also be influenced by the endothelial cells via generation of products including PG, NO and endothelin.
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PMID:Cellular biology of bone resorption. 850 94

In skeletal muscle, the Na+, K+ pump is predominantly situated in the sarcolemma (1000-3500 pumps per microns 2). The total concentration can be determined in fresh or frozen biopsies (1-5 mg) using a 3H-ouabain binding assay. The values obtained have been confirmed by measurements of maximum ouabain suppressible Na+, K(+)-transport capacity in intact muscles as well as Na+, K(+)-ATPase-related enzyme activity in muscle homogenates. In the mature organism, the concentration of Na+, K+ pumps varies with muscle type and species in the range 150-600 pmol (g wet wt)-1 in rat and human muscle, the concentration increases markedly with thyroid status. Semi-starvation and untreated diabetes reduce the concentration by 20-48%. K+ deficiency leads to a downregulation of up to 75%. Both in animals and in humans, training increases the concentration of Na+, K+ pumps in muscle and inactivity leads to a downregulation. High-frequency stimulation elicits up to a 20-fold increase in the net efflux of Na+ within 10 s This is the major activation mechanism for the Na+, K+ pump, utilizing its entire capacity and possibly represents a drive on de novo synthesis of Na+, K+ pumps. A variety of hormones (insulin, insulin-like growth factor I, adrenaline, noradrenaline, calcitonin gene-related peptide, calcitonin, amylin) increase the rate of active Na+, K+ transport by 60-120% within a few minutes. This leads to a decrease in intracellular Na+ and hyperpolarization. In isolated muscles, where contractility is inhibited by high extracellular K(+)- such agents produce rapid force recovery. which is entirely suppressed by ouabain and closely correlated to the stimulation of K+ uptake and the decline in intracellular Na+. The observations support the conclusion that the Na+, K+ pump plays a central role in the acute recovery and maintenance of excitability during contractile activity.
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PMID:The Na+, K+ pump in skeletal muscle: quantification, regulation and functional significance. 872 82

The study of osteoclast differentiation, function, and fate has been hampered by the lack of nonavian, nonrodent models in which biochemical and molecular studies can be conducted. The present study was undertaken to determine if osteoclasts could be generated from porcine bone marrow cells. Bone marrow from the long bones of neonatal female pigs was enriched for mononuclear cells and cultured in the presence or absence of 1,25-(OH)2D3, rhIL-11, or PGE2. A confluent layer of stromal cells was observed after 4-8 days in culture and multinucleated giant cells formed after 6-10 days of culture. The multinucleated cells stained positively for tartrate-resident acid phosphatase and formed resorption lacunae when exposed to bovine cortical bone slices. When examined by transmission electron microscopy, abundant mitochondria, perinuclear Golgi complexes, numerous variably sized vacuoles, prominent rough endoplasmic reticulum, and free polysomes were observed in the multinucleated cells. Stimulation of the in vitro generated osteoclasts with 10(-8) mol/L salmon calcitonin resulted in a three to fivefold increase in cAMP production and in cell retraction. Although the osteoclasts formed in the presence or absence of 1,25-(OH)2D3, 10-50-fold more osteoclasts were observed in the cultures treated with 1,25-(OH)2D3 in comparison to cultures without 1,25-(OH)2D3. Osteoclast differentiation was also stimulated by rhIL-11 and PGE2; although, the number of cells generated in 6-7 days was significantly less than the number obtained with 1,25-(OH)2D3, treatment. In addition, these multinucleated cells expressed high levels of Src kinase activity and responded to bafilomycin A1, an inhibitor of the vacuolar type H(+)-ATPase, treatment with a decrease in osteoclastic bone resorption. In summary, the porcine cells possess the major distinguishing characteristics of osteoclasts and provide an alternative mammalian model to study osteoclast differentiation and resorptive activity.
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PMID:Development and characterization of a porcine model to study osteoclast differentiation and activity. 887 68

The present study was performed to clarify the role of vacuolar H+-ATPase in the regulation of the intracellular pH (pHi) in osteoclasts. Bafilomycin A1 or amiloride were added to rat osteoclast cultures to block the H+-ATPases and Na+/H+-exchangers, respectively. Addition of 10(-8) M bafilomycin A1 to osteoclasts cultured on bone induced a rapid decrease of the pHi, while addition of amiloride had only a minor effect. The response to bafilomycin A1 appeared simultaneously with resorption activity and was abolished when resorption was inhibited by calcitonin. Osteoclasts on bone recovered from acid loading caused by propionate in the presence of amiloride, while bafilomycin A1 inhibited this recovery almost completely. The pHi of osteoclasts cultured on glass responded to the addition of amiloride, but was not effected by even high concentrations of bafilomycin A1. In contrast, as little as 10(-10) M bafilomycin A1 caused accumulation of large vesicles in the cytoplasm.
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PMID:The regulation of pHi in osteoclasts is dependent on the culture substrate and on the stage of the resorption cycle. 920 48

Calcitonin is a hormone peptide produced by the thyroid gland, whose best described role is to prevent bone reabsorption. It also participates in other biological functions, even at central nervous system level. We studied the effect of added calcitonin on ATPase and acetylcholinesterase activities in synaptosomal membranes isolated from rat cerebral cortex. Calcitonin at 10(-7) - 10(-5)M concentration decreased 20-40% Na+, K(+)-ATPase and 15-25% K(+)-p-nitrophenylphosphatase activities, and at 10(-6)-10(-5)M reduced 20-30% Mg(2+)-p-nitrophenylphosphatase activity. However, this peptide failed to modify Mg(2+) - and Ca(2+)-ATPase or acetylcholinesterase activities. Results suggest that the sodium pump may be a target for calcitonin effects at neuronal level. Thus, calcitonin inhibition of sodium/potassium transport through synaptic membranes supports a regulatory role of this peptide on neurotransmission.
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PMID:A study of calcitonin effect on synaptosomal membrane enzymes. 921 Jan 82

1. The vascular effect of insulin in the mesenteric resistance blood vessel and the role of calcitonin generelated peptide (CGRP)-receptor in insulin-induced vascular responsiveness were investigated in rats. 2. The mesenteric vascular beds isolated from Wistar rats were perfused with Krebs solution, and perfusion pressure was measured with a pressure transducer. In preparations contracted by perfusion with Krebs solution containing methoxamine in the presence of guanethidine, the perfusion of insulin (from 0.1 to 3000 nM) caused a concentration-dependent decrease in perfusion pressure due to vasodilatation. The pD2 value and maximum relaxation (%) were 6.94+/-0.22 and 43.9+/-5.2, respectively. 3. This vasodilator response to insulin was unaffected by 100 nM propranolol (beta-adrenoceptor antagonist) plus 100 nM atropine (muscarinic cholinoceptor antagonist), 100 microM L-NG-nitroarginine (nitric oxide synthase inhibitor), 1 microM ouabain (Na+-K+ ATPase inhibitor), or 1 microM glibenclamide (ATP sensitive K+-channel inhibitor). 4. In preparations without endothelium, perfusion of insulin produced a marked vasodilatation. The pD2 value and maximum relaxation (%) were 7.62+/-0.21 and 81.0+/-4.6, respectively, significantly greater than in preparations with intact endothelium. 5. The vasodilator responses to insulin in the preparations without endothelium were significantly inhibited by CGRP[8 37], a CGRP receptor antagonist, whereas pretreatment with capsaisin, a toxin for CGRP-containing nerves, did not affect insulin-induced vasodilatation. 6. These results suggest that insulin induces non-adrenergic, non-cholinergic and endothelium-independent vasodilatation, which is partially mediated by CGRP receptors.
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PMID:Involvement of calcitonin gene-related peptide (CGRP) receptors in insulin-induced vasodilatation in mesenteric resistance blood vessels of rats. 960 76

The ECL cells are peptide hormone-producing cells, rich in histamine and chromogranin A (CGA)-derived peptides, that operate under the control of gastrin. Gastrin and the ECL cells form a functional unit, the gastrin-ECL-cell axis. The aims of the present study were to examine (1) if calcitonin (CT), parathyroid hormone (PTH) and vitamin D affect the gastrin-ECL-cell axis (by measuring the activity of the histamine-forming enzyme, histidine decarboxylase (HDC), and the expression of HDC mRNA and CGA mRNA in the ECL cells), and (2) if activation of the gastrin-ECL-cell axis affects the parathyroid glands (by measuring plasma PTH and mRNA expression). We also examined the possibility that the oxyntic mucosa harbours vitamin D receptors. Fasted rats received intravenous infusion of PTH and CT with or without gastrin. PTH raised the blood Ca2+ concentration, whereas CT infusion lowered it. Plasma PTH rose in response to CT, while serum gastrin remained unaffected. ECL-cell HDC was activated by gastrin but not by CT and PTH. Five daily subcutaneous injections of large amounts of ergocalciferol raised the blood Ca2+ concentration, while reducing the oxyntic mucosal HDC activity and the expression of HDC and CGA mRNA. The serum gastrin concentration was not affected. The findings are in line with the idea that the gastrin-ECL-cell axis can be suppressed by vitamin D or by vitamin D-dependent mechanisms. Western blot analysis revealed the presence of vitamin D receptor immunoreactivity and reverse transcription PCR detected vitamin D receptor gene expression in the rat oxyntic mucosa. Hypergastrinemia was induced by daily peroral treatment with the H+/K+-ATPase inhibitor, omeprazole, for 2 weeks or by continuous subcutaneous infusion of gastrin for 7 days. Elevated serum gastrin concentration was associated with increased HDC activity and increased HDC and CGA mRNA expression in the oxyntic mucosa. There was no elevation of plasma PTH or PTH mRNA expression in the parathyroid gland.
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PMID:Rat stomach ECL-cell histidine decarboxylase activity is suppressed by ergocalciferol but unaffected by parathyroid hormone and calcitonin. 1010 Sep 26


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