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)

1. The activities of ATPase in rat CNS were studied 3 hr after administration of the noradrenaline uptake inhibitor, desipramine (DMI: 10 mg.kg-1, i.p.). Na+K+-ATPase activity significantly increased after DMI in the whole particulate from hypothalamus and mesencephalus but no changes in frontal cortex or in pons-medulla oblongata areas were found. This increase was prevented when the animals were pretreated with the noradrenergic neurotoxic N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4). 2. Purified membrane fractions from hypothalamus were obtained by differential and sucrose gradient centrifugation (0.8-1.2 M sucrose). It was observed that after DMI, Na+,K+-ATPase activity increased only in the membranous fraction lying at 0.9 M sucrose. 3. Mg2+- or Ca2+-ATPase activities were not modified by DMI treatment. 4. Citalopram, a specific serotonergic uptake inhibitor, did not affect ATPase activities. 5. The results obtained could indicate that DMI acute administration selectively stimulates Na+,K+-ATPase activity of certain membranes of the CNS after an increase in the concentration of the noradrenergic neurotransmitter in the synaptic gap.
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PMID:Stimulation of Na+,K+-ATPase activity in certain membranes of the rat central nervous system (CNS) by acute administration of desipramine (DMI). 254 51

The distribution of specific binding of [3H]dihydroalprenolol([3H]DHA) in sucrose gradients (0.2-1.75 M), containing homogenates of the cortex of rat brain, centrifuged to equilibrium (110,000 g/16 hr), was examined in controls and after treatment with antidepressant drugs. There were no significant changes in the specific binding of [3H]DHA after acute administration of desipramine (DMI, 50 mg/kg) or clorgyline (20 mg/kg), either in terms of the number of receptors or distribution in the sucrose gradient. There was a significant decrease (29%) in the number of beta-adrenoceptors after the chronic regimen with DMI, but again no apparent alteration in the density of the receptor-containing membranes, both samples having a maximum distribution at approximately 1.1 M sucrose. Non-specific binding was maximal at 0.65 M sucrose. Electron microscopy showed that the non-specific binding was largely to myelin and the fraction containing most specific binding was composed of membrane fragments. The activity of Na+ K+ ATPase had a single broad peak (maximum at 1.1 M sucrose). Thus, at the times studied, in vivo desensitisation/internalisation of cortical beta-adrenoceptors did not apparently occur following large acute doses of antidepressant drugs and furthermore the down-regulation which followed the chronic regimen with DMI did not involve migration of receptors into "light density fractions" which are reported to be present after acute exposure to agonists in vitro.
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PMID:Subcellular distribution of beta-adrenoceptors in brain following administration of antidepressant drugs. 282 64

This study examined the effects of diet and treatment with noradrenergic receptor antagonists on weight gain and indices of Na+-K+-adenosine triphosphatase (ATPase) activity in the rat. When rats were fed a palatable cafeteria diet, their caloric consumption increased by about 80%, but they did not gain weight significantly. Ouabain binding and K+-p-nitrophenylphosphatase (NPPase) activity were increased in brown adipose tissue and soleus. These indices remained elevated after the rats were returned to a regular diet. When rats were fasted for 3 days, they lost weight, and the indices of Na+-K+-ATPase activity were markedly reduced in brown adipose tissue and soleus. After refeeding the fasted rats gained weight three times more rapidly than nonfasted rats with similar food intake. Indices of Na+-K+-ATPase activity remained as low as they had been when the rats were fasting. There was a consistent negative correlation between weight gain per calorie eaten and brown adipose tissue NPPase activity. Changes in Na+-K+-ATPase could therefore be involved in the effects of overfeeding and fasting on metabolic efficiency. Desmethylimipramine binding was increased by cafeteria diet and decreased by fasting, consistent with changes in sympathetic nervous system activity. Treatment with prazosin, an alpha 1-noradrenergic receptor antagonist, reduced Na+-K+-ATPase in either control or cafeteria diet-fed rats but did not alter the effect of cafeteria diet feeding. By contrast, treatment with propranolol, a beta-receptor antagonist, prevented the increase in Na+-K+-ATPase during cafeteria diet feeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Caloric intake and Na+-K+-ATPase: differential regulation by alpha 1- and beta-noradrenergic receptors. 608 94

We examined the time course of K+-p-nitrophenylphosphatase and ouabain binding associated with cerebral cortex (Na+,K+)-AT-Pase after depletion of norepinephrine. Norepinephrine depletion by the norepinephrine-selective neurotoxin DSP4 initially reduced the indices of (Na+,K+)-ATPase, with a significant correlation between ouabain binding and tissue norepinephrine levels 16 h after DSP4. Tissue norepinephrine content and DMI binding rapidly declined after DSP4 and remained essentially unchanged for at least 8 weeks. By contrast, the indices of (Na+,K+)-ATPase remained low for about two weeks but then gradually increased, returning to baseline levels by 8 weeks after DSP4. These data indicate that, while usually regulated in part by exposure to norepinephrine, brain (Na+,K+)-ATPase undergoes adaptation to prolonged noradrenergic depletion.
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PMID:Brain (Na+,K+)-ATPase and noradrenergic function: recovery of enzyme activity after norepinephrine depletion. 609 36

We have previously shown that Na+, K(+)-ATPase activity in hypothalamus is increased after administration of an acute dose of desipramine, a noradrenaline uptake inhibitor (Viola et al., Cell Molec Neurobiol 9:263-271, 1989). In this report the same treatment (10 mg per kg) was applied to evaluate 3H-ouabain binding in rat brain sections by quantitative autoradiography. Results disclosed an increase in the number of ouabain binding sites in hypothalamus but not in cerebral cortex. Concomitantly, such acute DMI treatment enhanced K(+)-stimulated-p-nitrophenylphosphatase activity in hypothalamus membranes whereas it failed to modify cerebral cortex membranes. A direct interaction of DMI with the enzyme was ruled out since in vitro DMI is known to inhibit the enzyme. It may be speculated that DMI indirectly stimulates Na+, K(+)-ATPase through the increase in noradrenaline which acts in turn on the external phosphorylated site of the enzyme.
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PMID:Desipramine modulates 3H-ouabain binding in rat hypothalamus. 898 Dec 40

We used 28 crossbred wether lambs to determine the effects of dietary forage:concentrate ratio and metabolizable energy intake on visceral organ growth and oxidative capacity of gut tissues in lambs. Lambs were assigned randomly to a factorial arrangement of dietary treatments consisting of pelleted diets containing either 75% orchardgrass or 75% concentrate fed once daily at either .099 or .181 Mcal ME x (kg BW(.75))(-1) x d(-1). After a 52-d feeding period, lambs were slaughtered to obtain measurements of visceral organ mass and composition and oxidative capacity of isolated epithelial cells. Lamb performance, as measured by DMI, ADG, and efficiency of gain, was greater (P = .0001) for both diets at high ME intake. Likewise, lambs fed 75% concentrate gained faster and more (P < or = .01) efficiently than lambs fed 75% forage. Total digestive tract (TDT; includes rumen, reticulum, omasum, abomasum, and intestines) weight increased (P = .0001) with ME intake and was greater (P = .03) in lambs fed 75% forage than in those fed 75% concentrate. As a percentage of empty body weight (EBW), TDT weight increased with ME intake in lambs fed 75% forage, but it was unaffected by ME intake in lambs fed 75% concentrate (diet x intake, P = .03). Liver weight increased (P = .0001) with ME intake and was greater (P = .005) in lambs fed 75% concentrate vs 75% forage; however, liver weight as a percentage of EBW was increased (P = .0002) with ME intake but was unaffected by diet. Greater ME intake increased (P < or = .02) small intestinal (SI) epithelial and muscle mass of 15-cm sections, whereas jejunal epithelial mass was greater (P = .01) for lambs fed 75% forage vs 75% concentrate. Rumen epithelial concentrations of DNA and RNA increased (P < or = .02) with greater ME intake, whereas SI concentrations of DNA and RNA were largely unaffected by diet or ME intake. The activity of Na(+)-K(+)-ATPase increased in ileal epithelium (P < or = .02) with ME intake and concentrate in the diet, but activity in ruminal epithelium increased (P = .05) with concentrate. Total oxygen consumption by isolated ruminal and intestinal epithelial cells was unaffected by treatment. These data suggest that ME intake and level of dietary forage affect ruminal and intestinal growth via changes in cellular hyperplasia. Additionally, this study supports the concept that ME intake and diet composition alter gut energy expenditure, at least in part, through changes in mass rather than mass specific metabolism.
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PMID:Effects of diet forage:concentrate ratio and metabolizable energy intake on visceral organ growth and in vitro oxidative capacity of gut tissues in sheep. 1076 85