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 activity of the ouabain-sensitive Na+K+-ATPase may be reduced in primary hypertension by an ouabain-like humoral factor with resultant increase in intracellular Na+ and Ca2+ and peripheral vasoconstriction. To test this, we studied the forearm blood flow in 18 normotensive subjects. First, nifedipine, phentolamine, prazosin, sodium nitroprusside and ouabain were infused into the brachial artery. Secondly, each vasodilator was given in combination with ouabain. Blood pressure was measured directly, and blood flow by venous occlusion plethysmography. When nifedipine was combined with ouabain the elevation of vascular resistance was completely abolished. We detected no effect on the forearm veno-arterial difference for noradrenaline following intra-arterial infusion of drugs. If an ouabain-like factor plays a role in producing the elevated resistance of chronic hypertension, calcium entry blockers will act close to the site of this primary abnormality.
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PMID:Ouabain-induced elevation in forearm vascular resistance, calcium entry and alpha-adrenoceptor blockade, and release and removal of noradrenaline. 289 70

The augmentation by the cardioactive steroid acetylstrophanthidin of neurotransmitter release evoked by tyramine, and the dependence of the augmentation upon Na+, has been investigated in dog saphenous vein rings in which monoamine oxidase activity and uptake2 had been inhibited with pargyline and corticosterone respectively. High extracellular Na+ (Nao; 263 mmol/l) reduced basal efflux of 3H-compounds from the rings and also reduced tyramine-evoked efflux. Low Nao (25 mmol/l) increased basal efflux of 3H but reduced tyramine-evoked efflux. The increment in basal 3H-efflux caused by low Nao was cocaine-sensitive. A presumed increase in intracellular Na+ (Nai), produced by preincubating rings with acetylstrophanthidin in normal (143 mmol/l) or high Nao, augmented 3H-efflux evoked by subsequent incubation with tyramine in normal Nao. Pre-incubating rings with acetylstrophanthidin in low Nao, conditions which would not be expected to increase Nai, did not cause augmentation of the subsequent tyramine-evoked 3H-efflux. An increase in Nai, produced either as above or by pre-incubating rings in high Nao alone, reduced subsequent neuronal 14C-tyramine uptake. Low Nao present only during incubation reduced neuronal 14C-tyramine uptake, but high Nao present only during incubation did not increase neuronal 14C-tyramine uptake from that measured in normal Nao. The data are consistent with the following hypotheses: that tyramine uptake is dependent upon the prevailing inwardly directed Na+-gradient, that consequent noradrenaline efflux is Na+-gradient dependent and that the enhancement by acetylstrophanthidin of tyramine-evoked 3H-efflux is a consequence of the raised Nai caused by Na+,K+-ATPase inhibition.
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PMID:Augmentation of the indirect sympathomimetic action of tyramine by cardioactive steroids is a consequence of elevated intracellular sodium. 289 96

In order to test the hypothesis that Na+, K+-ATPase (Na+,K+-dependent ATPase) is involved in the noradrenaline-mediated stimulation of respiration in brown adipose tissue, the effects of noradrenaline on Na+,K+-ATPase in isolated brown-fat-cell membrane vesicles, and on 22Na+ and K+ (86Rb+) fluxes across the membranes of intact isolated cells, were measured. The ouabain-sensitive fraction of the K+-dependent ATPase activity in the isolated membrane-vesicle preparation was small and was not affected by the presence of noradrenaline in the incubation media. The uptake of 86Rb+ into intact hormone-sensitive cells was inhibited by 80% by ouabain, but it was insensitive to the presence of noradrenaline. 22Na+ uptake and efflux measured in the intact cells were 8 times more rapid than the 86Rb+ fluxes and were unaffected by ouabain. This indicated the presence of a separate, more active, transport system for Na+ than the Na+,K+-ATPase. This is likely to be a Na+/Na+ exchange activity under normal aerobic conditions. However, under anaerobic conditions, or conditions simulating anaerobiosis (2 mM-NaCN), the unidirectional uptake of Na+ increased dramatically, while efflux was unaltered.
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PMID:Regulation of Na+ transport in brown adipose tissue. 294 72

Hydralazine, a hypotensive agent, induces relaxation on smooth musculature. Several mechanisms related to membrane processes have been proposed to explain its relaxing action. In the present paper, the effects of hydralazine on ATPase activity in rat aorta have been studied. Hydralazine (10(-4)-5 X 10(-3) M concentration-dependently relaxed the isolated rat aortic arterial strips under norepinephrine-, serotonin- and K+-contractures. 5-Hydroxytryptamine contractures were more sensitive to the effects of hydralazine than noradrenaline- and potassium-contractures. We found that hydralazine does not modify ATPase activity on rat aorta homogenates. On the other hand, ATPase activity of rat aorta homogenates is dependent on divalent cations Ca2+ and Mg2+, and a little Na, K-ATPase activity was found.
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PMID:Hydralazine-relaxing effect on rat aorta is not mediated through changes in ATPase activity. 295 16

Vanadate (+5) is a potent inhibitor of a variety of ATPases including dynein ATPase. We describe a method useful for estimating the functional dissociation rate of vanadate from the active site which does not rely on classical physical separation techniques. The method involves spectrophotometrically monitoring the enzymatic activity as the inhibitor dissociates from the enzyme and is inactivated by norepinephrine. Norepinephrine effectively reverses vanadate inhibition by reducing vanadate (+5) to oxovanadium (+4). This reduction by norepinephrine is sufficiently fast for these purposes--addition of vanadate after norepinephrine shows no inhibition of ATPase activity. The mathematical estimation procedure is generally useful for estimation of dissociation rates of other reversible inhibitors which can be quickly inactivated after dissociation from the enzyme. The rate of dissociation of vanadate from dynein with ATP and 2-N3ATP as substrates using this method was estimated to be in the ranges 0.0023-0.0042 and 0.0057-0.0075 s-1, respectively. These rates permit estimation of the rates of vanadate association with dynein by using the reported dissociation constant for vanadate. The results are consistent with the very fast and potent inhibition of dynein ATPase activity observed.
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PMID:Kinetics of vanadate dissociation: estimation of the rate by inhibitor inactivation. 296 96

The interaction of noradrenaline, various cation chelators and calcium on Na+, K+-ATPase from rat cerebral cortex plasma membranes was studied. It was shown that chelation of inhibitory cations by EGTA, EDTA and dipyridyl activated Na+, K+-ATPase to the same extent as noradrenaline but at higher concentrations; increasing concentrations of EGTA depressed the activation by noradrenaline; calcium in the form of a calcium-EGTA buffer depressed Na+, K+-ATPase at physiological concentrations; the inhibition of Na+, K+-ATPase by calcium is dependent on the magnesium concentration in the assay and the inhibition by calcium was partially reversed by noradrenaline.
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PMID:The interaction between calcium and the activation of Na+, K+-ATPase by noradrenaline. 298 41

Norepinephrine (0.1 mM) has been reported to "sensitize" (Na+ + K+)-ATPase activity of rat brain homogenates to inhibition by ethanol. The present study extends these investigations to the mouse and includes other ATPase activities. We measured the effects of norepinephrine on the sensitivity of ethanol-induced inhibition of (Na+ + K+)-stimulated (E.C. 3.6.1.3), (Mg++)-dependent (E.C. 3.6.1.4) and (Ca++)-dependent ATPase activities. Whole forebrains from C57BL/6J mice were homogenized and assayed in vitro for ATPase activity using standard conditions. Ethanol (0.125-2.0 M) caused a dose-dependent inhibition of all three ATPases. Norepinephrine (0.1 mM) had no appreciable effect on ethanol's inhibition of (Na+ + K+)-stimulated or (Ca++)-dependent ATPase activities, but slightly antagonized ethanol's effect on (Mg++)-ATPase. These results suggest that norepinephrine has little effect on the sensitivities of specific ATPases to ethanol inhibition in mouse brain.
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PMID:Effect of norepinephrine on inhibition of mouse brain (Na+ + K+)-stimulated, (Mg++)-dependent, and (Ca++)-dependent ATPase activities by ethanol. 299 May

Inhibition of the Na,K-ATPase is known to cause transmitter release from many neurons. The mechanism of [3H]norepinephrine release was examined in primary cultures of sympathetic neurons. Ouabain caused [3H]norepinephrine release at concentrations that produced 80 to 90% inhibition of Na,K-ATPase activity. The effect of ouabain was compared with the effects of high K+ and the Ca2+ ionophore A23187. [3H]Norepinephrine release elicited by depolarization with high extracellular K+ was dependent on extracellular Ca2+, was unaffected by tetrodotoxin, was potentiated by reducing extracellular Na+, and was potentiated by the norepinephrine uptake inhibitor desipramine. These are the results expected if high K+ causes release by exocytosis, and if blockade of the Na+-dependent norepinephrine uptake system increases the net measurable release of the transmitter. The Ca2+ ionophore A23187 caused [3H]norepinephrine release that was not dependent on extracellular Ca2+ but which was like the release elicited by high K+ in other respects. Release elicited by ouabain was independent of extracellular Ca2+, was delayed for several hours by tetrodotoxin, was inhibited by reducing the concentration of extracellular Na+, and was inhibited by desipramine. These results suggest that the measured increase in transmitter release is secondary to a rise in the concentration of intracellular Na+. The data are consistent with the hypothesis that at high levels of pump inhibition, ouabain elicits nonvesicular [3H]norepinephrine release through reversal of the Na+-dependent plasma membrane carrier.
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PMID:Ouabain-evoked norepinephrine release from intact rat sympathetic neurons: evidence for carrier-mediated release. 299 43

The mechanism by which noradrenaline stimulates ouabain-sensitive rubidium uptake in guinea-pig myocardial tissue has been studied. The stimulatory action of low concentrations of noradrenaline was reversed by high doses of propranolol (10(-5) mol/l) in atrial tissue, but was not reversed by alpha- or beta-, or combined alpha- and beta- adrenoceptor antagonists in ventricular tissue. Rubidium uptake was also found to increase with increasing extracellular potassium concentration [( K]o). The percentage values of stimulation by noradrenaline decreased with increasing [K]o. Noradrenaline had no effect on the rate of ATP splitting by an isolated membrane preparation of Na,K-ATPase. It is proposed that noradrenaline stimulates active cation transport by either (a) an effect secondary to increased passive efflux of K ions, or (b) an action at a novel adrenergic receptor, distinct from the ATPase enzyme itself.
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PMID:The mechanisms of action of noradrenaline on ouabain-sensitive rubidium uptake in guinea-pig myocardium. 299 91

We examined effects of treatment with cardiac glycosides, in combination with noradrenergic stimulation or depletion, on (Na+,K+)-ATPase activity in rat cerebral cortex, heart, and kidney. Treatment with digitoxin increased the apparent number of (Na+,K+)-ATPase sites in heart, cerebral cortex, and kidney. Ouabain, which crosses the blood-brain barrier poorly, did not affect enzyme in brain but was otherwise similar. Norepinephrine depletion prevented the increase in heart but not in cerebral cortex. Noradrenergic stimulation increased the number of sites in cerebral cortex and in heart. In rats treated with digitoxin, noradrenergic stimulation increased enzyme activity further in heart but not in cerebral cortex. Examination of effects on noradrenergic receptor binding and on norepinephrine metabolite concentrations suggested that, while in heart cardiac glycosides appeared to increase norepinephrine release, in brain there was no effect on release but there may have been appreciable inhibition of norepinephrine reuptake under stimulated conditions.
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PMID:(Na+,K+)-ATPase and noradrenergic regulation: effects of cardiac glycoside treatment and noradrenergic manipulations. 300 19


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