Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chromaffin granules isolated from bovine adrenal gland were incubated with (3)H-labelled nucleotides and [(14)C]noradrenaline to study the uptake of these substances. [(3)H]ATP, [(3)H]ADP and [(3)H]AMP are taken up by these organelles by the same temperature-dependent mechanism. The apparent K(m) for ATP and ADP is 1.4mm, and for AMP it is 2.9mm. The uptake of ATP has a flat pH optimum, whereas the catecholamine uptake increases with more alkaline pH. Atractyloside and carboxyatractyloside are competitive and specific inhibitors of nucleotide uptake, whereas reserpine inhibits only that for catecholamines. Mg(2+) ions activate uptake of both catecholamine and nucleotides, whereas EDTA and N-ethylmaleimide inhibit these processes. Nucleotide and catecholamine uptakes are inhibited by uncouplers of oxidative phosphorylation and by two ATP analogues. NH(4) (+) ions and nigericin in the presence of KCl inhibit only catecholamine uptake. It is concluded that nucleotide uptake, as proposed previously for catecholamine uptake, depends on an electrochemical proton gradient produced by a proton-translocating adenosine triphosphatase localized in the membrane of chromaffin granules. Furthermore, as suggested by the effect of NH(4) (+) and nigericin, catecholamine uptake apparently depends on the chemical part of this gradient, whereas the results for nucleotide uptake are consistent with its dependence on the electrical component.
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PMID:A characterization of the nucleotide uptake of chromaffin granules of bovine adrenal medulla. 2 25

The effects of acute (10 mg/kg) and chronic 10 mg/kg for 30 days) administration of delta-9-tetrahydrocannabinol (delta9-THC) have been studied histochemically in the rat adrenal medulla, which include total catecholamines, noradrenaline, histometric measurements of adrenal medullary areas, calcium content of the medullary cells along with adenosine triphosphatase (ATPase), acetyl cholinesterase (AChE) and butyryl cholinesterase (BChE) activities. Acute delta9-THC treatment reduced the total catecholamine content (including noradrenaline) of the gland, was accompanied by increased ATP-ase, AChE, BChE activities and increased calcium distribution in the gland. Chronic delta9-THC treatment caused significant hypertrophy of the chromaffin tissue, with decreased total catecholamine content, although noradrenaline containing areas exhibited no notable change. The calcium content and ATPase activity were increased along with a concomitant increase in AChE and BChE activities. Although the changes in adrenal medullary enzyme activities following both acute and chronic delta9-THC treatment are qualitatively similar, marked quantitative increase is noted in the chronically treated groups. The results indicate an increased total catecholamine releasing activity of the adrenal medulla following acute delta9-THC treatment, while chronic delta9-THC administration produces a preferential release of adrenaline.
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PMID:Changes in rat adrenal medulla following delta9-tetrahydrocannabinol treatment. A histochemical study. 12 28

The catecholamine-stimulated adenosine triphosphatase (ATP-ase) activities in mouse brain synaptosomes were inhibited by morphine both in vitro and in vivo. Morphine up to 10(-3) M had no effect on basal ATPase activities but at 10(-4) M significantly inhibited dopamine-sensitive ATPase activities in vitro. The morphine effect was antagonized by an opiate antagonist, naloxone. The catecholamine-sensitive ATPase activities were also inhibited by acute administration of morphine. The inhibition was dose-dependent. However, naloxone partially antagonized the morphine inhibition of depamine-sensitive ATPase activity but not norepinephrine-sensitive ATPase activity. A significant decrease in the sensitivity of synaptosomal ATPase to catecholamines was observed in mice rendered tolerant by morphine pellet implantation. The Na+,K+-ATPase was more affected by morphine as compared to Mg++-ATPase activity. The dopamine-sensitive Na+,K+-ATPase activity was restored by 50% in precipitated withdrawal mouse brain synaptosomes. Norepinephrine-sensitive ATPase activity was also restored partially in precipitated withdrawal animals. These results suggest that in mouse brain synaptosomes morphine may be interacting with ATPase at or near the catecholamine-active sites.
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PMID:Effects of acute and continuous morphine administration on catecholamine-sensitive adenosine triphosphatase in mouse brain. 21 49

1. The contractile responses of aortic ring preparations from Sprague-Dawley rats made hypertensive by 6-week dietary salt loading were studied. The test and control diet contained 8.0 and 0.3% NaCl, respectively. Aortic rings from salt-loaded rats showed enhanced sensitivity to noradrenaline (NA) but not to serotonin. Contractile responses to CaCl2 in Ca-free NA-containing medium was significantly enhanced in salt-loaded rats, but was unchanged in K(+)-depolarised medium. K(+)-induced relaxation (a functional indicator of Na-K adenosine triphosphatase activity) was sensitive to 10 mumol/L ouabain and was significantly attenuated in aortic rings from salt-loaded rats. The results suggest that hypertension induced by salt-loading is associated with enhanced sensitivity to NA, increased Ca2+ entry through receptor-operated channels, and impairment of Na-K ATPase enzyme activity.
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PMID:Altered responses of aortic smooth muscle from Sprague-Dawley rats with salt-induced hypertension. 166 59

Using hepatocytes isolated by collagenase perfusion, we studied the accumulation of 3H-noradrenaline. Cells incubated during 15 min in the presence of 0.4 mumol/l 3H-noradrenaline (without inhibition of noradrenaline metabolism) accumulated 8.32 +/- 1.77 pmol/10(6) cells (n = 3). The accumulation of 3H-noradrenaline in isolated parenchymal liver cells was sensitive to 10 mumol/l cocaine (inhibition 36.6 +/- 7.9%, n = 3) and 1 mumol/l desipramine (inhibition 27.2 +/- 6.9, n = 3). Accumulation of 3H-noradrenaline was temperature and sodium dependent (inhibition 33.2 +/- 9.4%, n = 9, when Na+ was replaced by Tris+) and was influenced by the inhibition of the membrane Na(+)-K(+)-adenosine triphosphatase (Na(+)-K(+)-ATPase) by 150 mumol/l ouabain (34.7 +/- 6.9% inhibition, n = 3). Accumulation of 3H-noradrenaline in the hepatocytes was not affected by the presence of uptake2 inhibitors, normetanephrine (30 mumol/l) and corticosterone (30 mumol/l), but was reduced by 30 mumol/l isoprenaline (76.3 +/- 5.0% inhibition, n = 6). Thus, the system that takes up and accumulates noradrenaline in the isolated rat liver cells possesses some characteristics of both, uptake1 and uptake2 systems and appears to be different from other extraneuronal cocaine-sensitive systems, such as the one reported for pulmonary endothelial cells.
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PMID:Accumulation of 3H-(+/-)-noradrenaline by isolated rat liver cells. 216 96

1. The kidney taken from a rat rendered nephrotic by exposure to puromycin aminonucleoside retains sodium abnormally when perfused in isolation and has an abnormally low vascular resistance (J. D. Firth et al., Clin. Sci. 1989; 76, 387-95). In this study the relation of oxygen consumption to sodium reabsorption has been examined in the isolated nephrotic organ, which has also been exposed to a variety of natriuretic agents and to the effect of inhibition of metabolism by cooling, in an attempt to discern the transport process, or processes, responsible for abnormal tubular handling of sodium. In addition, the effects of three endogenous vasoconstrictors, noradrenaline, angiotensin II and endothelin, on the function of the isolated nephrotic kidney have been examined. 2. The ratio of mol of sodium reabsorbed by the tubules of the isolated nephrotic kidney to mol of oxygen consumed was reduced in comparison with the control kidney (means +/- SEM): 9.22 +/- 0.97 versus 15.43 +/- 1.55 (P less than 0.002). 3. In the presence of ouabain (1 mmol/l), acetazolamide (1 mmol/l), frusemide (200 mumol/l), the combination of these three agents together, hydroflumethiazide (100 mumol/l), benzamil (100 nmol/l) or atrial natriuretic peptide (1000 pmol/l), a lesser increment in sodium excretion was induced in the isolated nephrotic kidney than in the control kidney and the nephrotic organ continued to excrete less sodium in both absolute and fractional terms. 4. This suggests that enhanced tubular sodium reabsorption in the isolated nephrotic kidney does not depend upon abnormally increased activity of the Na+/K(+)-adenosine triphosphatase, bicarbonate-dependent sodium transport, Na+/K+/2Cl- co-transport, electrically neutral proportionate reabsorption of sodium and chloride (distal tubule), epithelial sodium channel (distal tubule) or atrial natriuretic peptide-sensitive sodium transport processes. 5. When isolated nephrotic kidneys and normal kidneys were cooled to 8-10 degrees C the handling of sodium became virtually identical in the two groups. On re-warming to 37 degrees C, the original differences in sodium handling between nephrotic and control kidneys were restored. This implies that the mechanism responsible for the abnormal tendency to retain sodium is temperature-sensitive; as yet it remains otherwise undefined. 6. The sensitivity of the renal vessels to noradrenaline, angiotension II and endothelin, as judged by the percentage reduction in perfusate flow rate produced by a given concentration of any of these agents, was not substantially altered in the nephrotic kidney compared with the control kidney. Increase in vascular tone was not associated with amelioration of the tendency of the isolated nephrotic organ to retain sodium. Increasing concentrations of angiotensin II caused the filtration rate to increase in the nephrotic kidney. This effect was unexpected: in the control preparation, as anticipated, angiotensin II caused the filtration rate to decrease.
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PMID:Effect of natriuretic agents, vasoactive agents and of the inhibition of metabolism on sodium handling in the isolated perfused kidney of the nephrotic rat. 217 43

1. The present studies were undertaken to investigate whether intracisternal administration of pergolide, a dopamine-2 receptor agonist, triggers the release of an inhibitor of ouabain-sensitive sodium, potassium-dependent adenosine triphosphatase into the circulation and whether such an effect is associated with increases in vascular reactivity in pentobarbital anaesthetized dogs. In different groups of animals, Na+-pump activity was estimated in the plantar and dorsal branches of the lateral saphenous veins by using the 86Rb-uptake method; vascular responsiveness to noradrenaline was studied in the denervated perfused hindlimb. 2. Na+-pump activity was significantly depressed in those blood vessels which were collected at 90 min after central administration of pergolide (12.5 micrograms/kg intracisternally). In perfused hindlimb studies, vascular responses to noradrenaline were significantly enhanced between 60 and 90 min after pergolide. Since the Na+-pump activity was evaluated in the hindlimb veins, and vascular reactivity was studied on the arterial circulation, the data suggest that the changes in both these variables could have been caused by a circulating substance. 3. In separate series of experiments, plasma samples were collected before and after intracisternal administration of pergolide. The Na+-pump activity was significantly inhibited in the segments of lateral saphenous veins which were incubated in the fresh plasma and/or boiled plasma supernatants, indicating that a heat stable pump inhibitor(s) is released into the circulation after pergolide administration. 4. Effects of pergolide demonstrated in the present study are qualitatively similar to those reported to occur after acute blood volume expansion. Hence it is proposed that central dopaminergic mechanisms may play an intermediary role in the release of the Na+-pump inhibitor(s).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracisternal administration of pergolide, a dopamine receptor agonist, triggers the release of an inhibitor of ouabain-sensitive sodium, potassium-dependent adenosine triphosphatase and enhances vascular reactivity in anaesthetized dogs. 244 97

Low sodium and potassium adenosine triphosphatase (ATPase) activity has been proposed as a mechanism behind diabetic neuropathy. In this study the platelet ATPase activity and platelet noradrenaline efflux rate were determined in 47 insulin-dependent diabetes mellitus (IDDM) patients and 20 controls. Ulnar motor conduction velocities, tested in a subgroup, were lower in patients than in controls (52.7 +/- 1.3 m s-1 vs. 61.3 +/- 1.4 m s-1; P less than 0.001). Platelet ATPase activity tended to be increased in the patients compared with the controls (29.9 +/- 1.0 x 10(-3) min-1 vs. 26.9 +/- 1.1 x 10(-3) min-1; NS). In ulnar nerve function tested subjects, ATPase activity was higher in patients than in controls (31.2 +/- 1.7 x 10(-3) min-3 vs. 25.9 +/- 1.3 x 10(-3) min-1; P less than 0.01). The platelet noradrenaline efflux rate tended to be higher in patients with lower brake indices, a sign of autonomic neuropathy, than in controls (29.0 +/- 3.0 x 10(-3) min-1 vs. 21.2 +/- 0.9 x 10(-3) min-1; P less than 0.05). The platelet ATPase activity was not decreased in IDDM patients, however, a connection between diabetic autonomic neuropathy and platelet transmittor leakage was indicated.
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PMID:Platelet sodium and potassium ATPase [corrected] activity and noradrenaline efflux rate in relation to autonomic and peripheral nerve function in insulin-dependent diabetic patients. 253 27

An experimental model of myocardiopathy was induced in rhesus monkeys following noradrenaline (NA) infusion (20 ug/kg body wt/minute), for a period of 2 hours daily for three consecutive days. The animals were sacrificed after two hours (acute phase), forty-eight hours (sub-acute phase) and twenty-one days (chronic phase). Focal depletion of succinic dehydrogenase, increase in adenosine triphosphatase, acid phosphatase and appearance of large fat droplets in myocardial muscle was noted in the acute phase. Histopathological examination revealed focal edema, opacity and fuchsinorrhagia of the muscle fibres distributed in both the ventricles. Myofibrillar degeneration, myocytolysis and vacuolization with aggregation of lymphomononuclear cells were the significant features in the acute phase. During sub-acute and chronic phases, these features became less prominent and reparative changes with proliferation of fibroblasts became more marked. By the twenty-first day, irregular, focal scars replaced the necrosed myocardium. Ultrastructurally, heart muscle showed myofibrillar disorganisation, distortion of Z and A bands, dilatation of sarcoplasmic reticulum and swelling and rupture of mitochondria. Altered membrane permeability was evidenced by the presence of reaction products of horseradish peroxidase within the cardiac cells. In the reparative phase, however, myocytolytic changes regressed and collagen deposition was the prominent feature. This experimental study has several histological features simulating human cases of myocardial infarction without coronary occlusion.
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PMID:Catecholamine-induced experimental cardiomyopathy--a histopathological, histochemical and ultrastructural study. 259 40

Effects of K+, ethanol and norepinephrine on the binding kinetics of ouabain to (Na+,K+)-adenosine triphosphatase in beef brain microsomes were examined. K+ reduced the rate and apparent affinity for ouabain binding markedly. Whereas ethanol and norepinephrine themselves inhibited ouabain binding slightly, they stimulated binding in the presence of K+. Norepinephrine enhanced the effect of ethanol. Dissociation of ouabain was biphasic, with fast and slow components corresponding to high and low apparent affinity. About 65% of the enzyme had high affinity, regardless of conditions. Norepinephrine and ethanol had differential effects on the rate of dissociation from high and low affinity enzyme, however. Alpha receptor blockade generally prevented the effects of norepinephrine. These results show that, although norepinephrine and ethanol have a modest effect on the amount of enzyme that can bind ouabain, their main effect on (Na+,K+)-adenosine triphosphatase is to antagonize the binding of K+ to its allosteric site that inhibits ouabain binding. The data support the hypothesis that ouabain binds rapidly to a K+-insensitive form of phosphorylenzyme or to its dephosphorylated analog and dissociates rapidly from E1.
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PMID:Ouabain binding to brain (Na+,K+)-adenosine triphosphatase: interactions of K+, ethanol and norepinephrine with high- and low-affinity binding. 302 3


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