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)

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

Rat C6 glioma cells were cultured for 4 days in MEM medium supplemented with 10% bovine serum and Na+, K+-ATPase activity was determined in homogenates of harvested cells. Approximately 50% of enzyme activity was attained at 1.5 mM K+ and the maximum (2.76 +/- 0.13 mumol Pi/h/mg protein) at 5 mM K+. The specific activity of Na+, K+-ATPase was not influenced by freezing the homogenates or cell suspensions before the enzyme assay. Ten minutes' exposure of glioma cells to 10(-4) or 10(-5) M noradrenaline (NA) remained without any effect on NA+, K+-ATPase activity. Neither did the presence of NA in the incubation medium, during the enzyme assay, influence the enzyme activity. The nonresponsiveness of Na+, K+-ATPase of C6 glioma cells to NA is consistent with the assumption that alpha (+) form of the enzyme may be preferentially sensitive to noradrenaline. Na+, K+-ATPase was inhibited in a dose-dependent manner by vanadate and 50% inhibition was achieved at 2 x 10(-7) M concentration. In spite of the fact that Na+, K+-ATPase of glioma cells was not responsive to NA, the latter could at least partially reverse vanadate-induced inhibition of the enzyme. Although the present results concern transformed glial cells, they suggest the possibility that inhibition of glial Na+, K+-ATPase may contribute to the previously reported inhibition by vanadate of Na+, K+-ATPase of the whole brain tissue.
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PMID:Na+, K+-ATPase activity in cultured C6 glioma cells. 254 85

Although active transport of potassium into human platelets has been demonstrated previously, there is hitherto no evidence that human platelets have an ouabain-inhibitable Na-K ATPase in their membrane. The present study demonstrates active rubidium (used as an index of potassium influx), 86Rb(K), influx into platelets, inhibitable by ouabain, and also demonstrates the presence of specific [3H]ouabain binding by the human platelet. This 86Rb(K) influx was stimulated by adrenaline, isoprenaline, and salbutamol, but noradrenaline caused a mild inhibition. Active 86Rb(K) influx by platelets was inhibited markedly by timolol, mildly by atenolol, but not by phentolamine. Therefore, active 86Rb(K) influx in human platelets is enhanced by stimulation of beta adrenoceptors of the beta 2 subtype. The platelet may therefore replace the leukocyte in future studies of Na-K ATPase activity. This would be a considerable advantage in view of the ease and rapidity of preparation of platelets.
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PMID:86Rb(K) influx and [3H]ouabain binding by human platelets: evidence for beta-adrenergic stimulation of Na-K ATPase activity. 254 65

Effect in vitro of benthiocarb, an organocarbamate herbicide on neonate rat (3 day old) brain was studied to understand the interaction of benthiocarb with Na+K+-ATPase. Na+K+-ATPase of the developing rat brain was selected as an index enzyme since alterations in the Na+K+-ATPase activity leads to neuronal dysfunction. The assay of Na+K+-ATPase in the presence of 1-8 mu moles of benthiocarb showed decreased activity and a concentration dependent inhibition of Na+K+-ATPase was noticed upto 7 mu moles of benthiocarb. Based on IC50 values (median concentration), 50% inhibition of the enzyme was observed with 5 mu moles of benthiocarb. Norepinephrine (NE) was selected to study the modulation of benthiocarb inhibited enzyme. Maximum increase (76.7%) of Na+K+-ATPase was noticed with 35 mu moles of NE and effective concentration (EC50) of NE which produced 50% activation of the enzyme was found to be 20 mu moles. This study suggests that NE acts as a protective agent in reversing the benthiocarb in vitro inhibited neonate rat brain Na+K+-ATPase.
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PMID:Modulation of benthiocarb in vitro inhibited neonate rat (Wistar strain) brain Na+K+-ATPase by norepinephrine. 255 4

We investigated interactions between noradrenaline and thyroid hormone status in the regulation of (Na+,K+)-ATPase in vivo. Treatment with the beta-adrenoceptor antagonist propranolol or with the neurotoxin 6-hydroxydopamine did not prevent the increases in heart (Na+,K+)-ATPase associated with triiodothyronine treatment. Administration of methimazole did not prevent the increase in (Na+,K+)-ATPase indices in cerebral cortex and heart associated with subacute noradrenergic stimulation by yohimbine. There was no evidence for synergistic effects between thyroid hormone administration and noradrenergic stimulation by yohimbine. Thyroid hormone, unlike noradrenaline, mainly increased (Na+,K+)-ATPase activity with low affinity for ouabain. These results show that noradrenaline and thyroid hormone regulate (Na+,K+)-ATPase by largely independent mechanisms, and may regulate different populations of enzyme molecules.
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PMID:Noradrenaline and thyroid function regulate (Na+,K+)-adenosine triphosphatase independently in vivo. 255 49

The present study aimed to elucidate the role of Na, K-ATPase inhibitor in renal sodium metabolism in essential hypertension. Mean arterial pressure (MAP), heart rate(HR), urine volume (UV), urinary excretion of sodium (UNaV), endogenous creatinine clearance (Ccr), fractional excretion of sodium (FENa), plasma renin activity(PRA) plasma aldosterone concentration(PAC), plasma noradrenaline concentration (PNA) and urinary excretion of noradrenaline(UNA) were measured before and after intravenous injection of ouabain (0.1 mg/m2.BSA) in 12 normotensive(NT) and 22 mild-to-moderate essential hypertensive subjects(EHT). Following ouabain injection, UV, UNaV FENa significantly increased, but PRA decreased, in both NT and EHT. MAP, HR, Ccr, PNA, and UNA did not change significantly in either group. On the other hand, a significant decrease in PAC was observed in NT, but not in EHT. The changes of UNaV and FENa were significantly attenuated in EHT as compared to NT. No significant difference in change of MAP, HR, UV, Ccr, PNA, UNA, or PRA was demonstrated between NT and EHT. A significantly positive correlation was found between delta UNaV and delta FENa in both NT and EHT, while no significant correlation was observed between delta UNaV and delta MAP, delta UV, delta Ccr, delta PRA, delta PAC, delta PNA and delta UNA in either group. These results suggest that 1) Na, K-ATPase inhibitor clearly augments natriuresis by suppression of sodium reabsorption in renal tubules, 2) since this augmentation was attenuated, there is an elevation of endogenous Na, K-ATPase inhibitor(s) should be considered in EHT, and 3) an increase of the inhibitor might participate to the hypertensive mechanism in EHT.
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PMID:[The role of the Na, K-ATPase inhibitor in renal sodium handling in patients with essential hypertension]. 255 14

p-Bromophenacyl bromide (PBPB), quinacrine and indomethacin, which inhibit phospholipase A2 (PLA2; EC 3.1.1.4) activity in several tissues, caused a dose-dependent inhibition of prelabelled [3H]noradrenaline ([3H]NA) release evoked by high concentrations of K+ from rat cerebral cortical synaptosomes. Release of prelabelled [3H]NA was caused by natural lysophosphatidic acid (LPA; 10(-6)-10(-5) g mL-1) and lysophosphatidylcholine (LPC; 10(-6)-10(-5) g mL-1) and synthetic LPA (6 x 10(-6), 2 x 10(-5) M) and LPC (6 x 10(-6), 2 x 10(-5) M), but not by natural lysophosphatidylserine (LPS; 10(-5) g mL-1), lysophosphatidylethanolamine (LPE; 10(-5) g mL-1) and lysophosphatidylinositol (LPI; 10(-5) g mL-1). The release evoked by natural LPA and LPC could be inhibited only marginally by PBPB and quinacrine. Phosphatidic acid (PA)-specific and phosphatidylcholine (PC)-specific PLA2 activities from rat cerebral cortical synaptosomes were stimulated in incubation medium containing high concentrations of K+ or calcium ionophore A23187. Low concentrations of PLA2 (10(-6)-10(-8) g mL-1, from bee venom) inhibited the synaptic membrane Na+,K+-ATPase activity in incubation media with intracellular levels of free Ca2+. Several lysophospholipids (LPLs), metabolites of the PLA2 type, also inhibited the synaptic membrane Na+,K+-ATPase activity in a dose-dependent manner. The minimum effective concentrations of natural LPA, LPC, LPS, LPI and LPE were 10(-6), 4.7 x 10(-6), 10(-5), 4.7 x 10(-5) and 4.7 x 10(-5) g mL-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of Na+,K+-ATPase activity by phospholipase A2 and several lysophospholipids: possible role of phospholipase A2 in noradrenaline release from cerebral cortical synaptosomes. 257 Aug 49

The identical increase of Na, K-ATPase activity is caused by oxidated and reduced forms of noradrenaline, serotonin and dopamine through the synaptosomal activating factors. The synaptosomal inhibiting factor, orthovanadate and calcium ions independently inhibit Na, K-ATPase activity. The inhibition constant (Ki) for vanadate does not change in the presence of EDTA, whereas in the presence of synaptosomal factors regulating the Na, K-ATPase factors, noradrenaline causes drastic increase of Ki for vanadate. It has been concluded, that the data point to the existence of special regulating system of brain synaptosomal Na, K-ATPase.
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PMID:[Regulation of Na,K-ATPase by synaptosomal factors and neurotransmitters]. 257 61

1. The interaction of ouabain, a Na+/K+ adenosine 5'-triphosphatase inhibitor, with sympathetic mechanisms of vasoconstriction, as well as its possible site(s) of action, were investigated in forearm arterioles of patients with uncomplicated hypertension. 2. Intra-arterial infusion of ouabain per se decreased forearm blood flow without changes in systemic arterial pressure or contralateral flow. However, the vasoconstrictor effect of the glycoside was abolished after local pretreatment with either phentolamine, a competitive alpha-adrenoceptor antagonist, or bretylium tosylate, a neurotransmitter blocker. 3. To exclude a non-specific effect due to the vasodilatation, a similar protocol was performed using histamine, which acts independently of sympathetic mechanisms. The vascular effect of ouabain was maintained in spite of histamine-induced increases in forearm blood flow even greater than those obtained from either blocker. 4. To discriminate between pre- and post-synaptic site(s) of action of ouabain, exogenous noradrenaline was infused intra-arterially after inactivation of local neurotransmitter release by bretylium, thus causing direct postsynaptic vascular alpha-adrenoceptor stimulation. Under these conditions, noradrenaline decreased forearm blood flow irrespective of the presence or absence of ouabain. 5. Thus, local sympatholysis by drugs acting on different levels of the sympathetic neuroeffector junction abolished the effect of ouabain, whereas histamine did not influence it. The data provide positive evidence for an effect of ouabain on sympathetically mediated vasoconstriction. This action is apparently not exerted at a postsynaptic site but possibly by enhancing neurotransmitter release. 6. If a circulating endogenous ouabain-like Na+/K+ adenosine 5'-triphosphatase inhibitor is relevant to the development of hypertension in man, it might act through a similar mechanism.
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PMID:Sympathetic vasoconstriction as a mechanism of action of ouabain in forearm arterioles of hypertensive patients. 258 25

Genetic hypertension in the rat is associated with abnormal renal function. This may be due to systemic hypertension or to intrinsic alterations in the kidney. Therefore, we examined intrinsic rates of oxidative metabolism in renal cortical tubules isolated from spontaneously hypertensive rats (SHR) and age-matched normotensive controls (WKY) before, during, and after the development of hypertension. We examined tubule function in SHR and WKY treated with antihypertensive agents to block the development of hypertension. During the early phase of hypertension (ages 7-8 wk), SHR tubules have intrinsic rates of oxygen consumption that are 15-25% greater than that of WKY. Ouabain-sensitive rates of oxygen consumption, an index of sodium entry, and Na+-K+-ATPase activity were not increased by 17%. Reduction of blood pressure with drugs did not abolish these differences in oxidative metabolism. Addition of exogenous arachidonic acid (1 microM) did reduce the metabolic differences between 8-wk-old SHR and WKY tubules. Norepinephrine (1 microM) had a greater stimulatory effect on oxygen consumption rates in tubules from hypertensive SHR. The relationship of these metabolic differences to the development of hypertension remains unclear.
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PMID:Increased oxidative metabolism in renal tubules from spontaneously hypertensive rats. 258 84


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