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PubMed1985

Indirect effects of adenosine triphosphate on chloride secretion in mammalian colon.

The effects of adenosine triphosphate (ATP) on short-circuit current (SCC) in rat colonic epithelium are described. ATP caused a large increase in inward-going current and was considerably more potent in this respect than ADP, AMP or adenosine. The response to ATP was sided, there being only minor effects when the nucleotide was added to the apical side of the tissue. The effects of ATP were not modified by the cyclooxygenase inhibitor, indomethacin, eliminating eicosanoid formation as a mechanism. The effects of ATP were potentiated by theophylline and not blocked by alpha, beta-methylene ATP. The data are consistent with the effect being dependent on the activation of adenylate cyclase, but it has not been possible to classify the receptors into P1 or P2 categories. Using inhibitors of NaCl cotransport (piretanide), carbonic anhydrase (acetazolamide), and chloride channels (diphenylamine-2-carboxylate), it was concluded that the SCC response to ATP was due to chloride secretion with, perhaps, a minor contribution from bicarbonate. Flux measurements with 22Na and 36Cl confirmed this view, there being approximate equivalence of chloride secretion with the SCC responses. Additionally, flux measurements revealed an inhibition of electroneutral NaCl absorption in response to ATP. The effects of ATP were antagonized by tetrodotoxin (TTX), greater than 50% inhibition being achieved with 10 nM TTX. This result suggests that ATP does not act directly on receptors in the epithelial cells but rather on neuronal elements in the lamina propria. It will be necessary to re-examine other secretagogues for indirect effects of this kind and to search for the final effector neurotransmitter which evokes secretion.

1-Methyl-3-isobutylxanthine↗

PubMedDate not supplied

Regional differences in noradrenaline-induced release of adenosine triphosphate from rat vascular endothelium.

We examined the release of endogenous adenyl purines such as adenosine triphosphate (ATP), ADP, AMP and adenosine from the caudal artery (CA), saphenous artery (SA), renal artery (RA), mesenteric artery (MA), pulmonary artery (PA) and thoracic aorta (TA) of rats, using high-performance liquid chromatography fluorescence detection. Noradrenaline induced the release of adenyl purines from these blood vessels. The total amount of adenyl purines release induced by noradrenaline from the CA was considerably larger than that from the TA. The rank order of the amount of adenyl purines released from the six blood vessels was CA>SA>RA>MA>PA> or =TA. The noradrenaline induced release of adenyl purines from the CA was significantly reduced by the removal of the endothelium. Noradrenaline also induced the release of adenyl purines from cultured endothelial cells of the CA and TA. The total amount of adenyl purines released from the former blood vessel was much larger than that from the latter. These results suggest the existence of vascular endothelial cells that are able to release ATP by an alpha1-adrenoceptor mediated mechanism, and that these cells are not homogeneously distributed in the vasculature.

Adenosine Triphosphate↗

PubMed1975

Adenosine triphosphate: nicotinamide mononucleotide adenylyltransferase of pig liver. Purification and properties.

Adenosine triphosphate : nicotinamide mononucleotide adenylyltransferase (EC 2.7.7.1) has been purifiec approximately 3500-fold from an extract of pig liver nuclei to a specific activity of 40 mumol of NAD+ per min per mg protein. The enzyme was found to have a molecular weight of 203 000, a frictional ratio of 1.6 and an isoelectric point of approximately 5. Michaelis constants for ATP and NMN were 0.11 mM and 0.12 mM, respectively.

Adenosine Triphosphate↗

PubMed1993

Adenosine triphosphate in the treatment of supraventricular tachycardia.

The efficacy of adenosine triphosphate (ATP, Spofa) in controlling supraventricular tachycardia (SVT) was assessed in a group of 20 consecutive patients with this condition. Sinus rhythm was restored in a total of 19 patients (95% efficacy). SVT termination was followed, in a full 40% of patients, by asystole with a mean duration of 8.6 seconds; there were, however, no sequelae and no measures had to be taken. ATP can be regarded as a welcome addition to the current range of pharmacological options available for the treatment of SVT.

Adenosine Triphosphate↗

PubMed1965

SEROTONIN AND ADENOSINE TRIPHOSPHATE: SYNERGISTIC EFFECT ON THE BEAT FREQUENCY OF CILIA OF MUSSEL GILLS.

For each tenfold increase in the concentration of serotonin in the range 10(-7) to 10(-4)M, the beat frequency of the lateral cilia of the gills of the freshwater mussel Elliptio complanatus increases by approximately two beats per second over the mean frequency of 14.5 beats per second for control gills perfused with 0.04M potassium chloride. The addition of 10(-6) to 10(-3)M concentrations of adenosine triphosphate has no detectable effect on the beat frequency. The addition of both serotonin and 10(-4)M adenosine triphosphate increases the frequency by two beats per second more than does the addition of serotonin alone.

Adenosine Triphosphate↗

PubMed1990

Adenosine triphosphate liposomes: encapsulation and distribution studies.

Four methods for encapsulating adenosine triphosphate (ATP) in liposomes were evaluated. Optimum entrapment required emulsifying ATP with the lipids used to form the liposome membrane in a high-speed homogenizer followed by evaporating the organic solvent with vigorous stirring. Under these optimum conditions ATP entrapment was 38.9%; i.e., the dosage form contained 38.9 g of ATP per 100 g of lipid. The distribution of positively charged liposomes loaded with ATP was studied in dogs with experimentally induced myocardial infarction. Intravenous injection of positively charged ATP liposomes caused accumulation of ATP in myocardial infarct tissue. Myocardial infarct tissue has reduced blood flow; since positively charged liposomes accumulated in infarct tissue, liposomes may be a drug delivery system for this disease state.

Adenosine Triphosphate↗

PubMed1984

The effect of anaerobiosis on adenosine triphosphate levels in larval Nippostrongylus brasiliensis and Haemonchus contortus.

The adenosine triphosphate (ATP) content of the pre-parasitic stages of Nippostrongylus brasiliensis, Haemonchus contortus (L1, L2 and L3) and the adults of the free-living nematode, Panagrellus redivivus, have been measured by bioluminescent photometry in aerated or near-anoxic conditions. The ATP content of the L1 and L2 stages of both parasitic species was unaltered by a lack of oxygen over a 90-min period. However, the L3 stage of both species and the adults of P. redivivus showed a significant fall in the level of ATP within 10 min of near-anoxia. This lower level of ATP was maintained during oxygen lack but the initial content was restored on return of the nematodes to aerobic conditions. The results suggest that measurement of ATP by bioluminescent photometry offers a readily measured and sensitive indicator of the capacity of a nematode to cope with transient changes in oxygen supply without undue metabolic stress.

Adenosine Triphosphate↗

PubMed2004

Cochlear administration of adenosine triphosphate facilitates recovery from acoustic trauma (temporary threshold shift).

BACKGROUND: Adenosine triphosphate (ATP) has often been used in the treatment of acoustic trauma although evidence supporting its clinical use was lacking. The aim of this study was to evaluate the chronic effects of ATP on acoustic trauma in guinea pigs. METHODS: We infused ATP into the perilymph of the guinea pig cochlea concurrently with intense noise exposure to investigate the effect of ATP on the process of recovery after acoustic trauma. We assessed auditory brainstem response (ABR) thresholds to evaluate cochlear function. RESULTS: After noise exposure (120 dB SPL, 5 h), ABR thresholds showed an increase of approximately 50 dB SPL that returned to normal after 14 days. Cochlear function in ATP-treated ears recovered more quickly than in control ears. The effect of ATP was inhibited by the administration of the ATP receptor antagonist: pyridoxal- phosphate-6-azophenyl-2',4'-disulfonic acid. CONCLUSION: These results suggest that ATP mitigates the effects of noise trauma through the ATP receptor.

Adenosine Triphosphate↗

PubMed1993

[The usefulness of adenosine triphosphate in supraventricular paroxysmal tachycardias].

With the objective to evaluate adenosine triphosphate (ATP) usefulness in supraventricular paroxysmal tachycardia (SPT), doses of 0.25 mg/kg, of ATP are administered fastly i.v. in bolus, to fifty consecutive patients with SPT resistant to vagal stimulation maneuvers. The effect achieved allowed to identify two groups: a) 39 patients in whom tachycardia was interrupted; b) 11 patients in whom tachycardia did not cease, but the induced transient provoked atrial-ventricular (A-V) blockage allowed to identify the underlying mechanism of tachycardia (in 6 of them atrial tachycardia and in 5 atrial flutter). In both groups the ATP effect was present in less than 30 seconds. In seven patients (five from group (a) and two from group b) the QRS duration was over 0.12 s. Six patients had a left ventricular ejection fraction below 30%. Side effects were frequent, but always short. ATP could become the drug of choice in the treatment of SPT without response to vagal maneuvers, due to the fact that, to its therapeutic activity, it must be added its diagnostic usefulness, its fast action and metabolization, together with the fact that it does not induce severe side effects.

Adenosine Triphosphate↗

PubMed1987

Permeability of red-cell membrane to adenosine triphosphate (ATP) molecules during hemorrhagic shock.

The findings of decreased adenosine triphosphate (ATP) levels in liver, kidney, and other tissues of animals in hemorrhagic shock were the rationale for previous experimental attempts to improve cell function by administration of fluids that contained high concentrations of ATP. The beneficial effects of this resuscitation, which are still controversial, were attributed to cellular uptake of ATP--it was assumed that cell membranes are permeable to this substrate. The effect of a high concentration of ATP in extracellular medium on intracellular ATP content was studied by using red blood cells (RBCs) from rabbits in control (normal) and in hemorrhagic shock states. The glucose-depleted RBCs were incubated in medium with 5 mMol/L ATP, and their ATP concentration fell markedly to the same level as seen in glucose-depleted RBCs incubated without ATP. The decrease of ATP in glucose-repleted RBCs, incubated with or without ATP, also did not show any significant difference. Similar to parallel experiments that used normal RBCs, the high extracellular ATP content did not substantially affect the intracellular ATP concentration in RBCs from animals in shock. This study indicates that ATP molecules in extracellular medium cannot penetrate either the normal RBC membrane or the RBC membrane during shock.

Adenosine Triphosphate↗

PubMed1979

An active-site-directed adenosine triphosphate analogue binds to the beta-subunits of factor F1 mitochondrial adenosine triphosphatase with its triphosphate moiety.

The reaction of the mixed anhydride of [3H]ATP and mesitylenecarboxylic acid and soluble mitochondrial adenosine triphosphatase is accompanied by the covalent binding of one molecule of the inhibitor to a molecule of the enzyme and results in the inhibition of adenosine triphosphatase activity by more than 90%. The electrophoresis of adenosine triphosphatase modified by reaction with the mixed anhydride of [3H]ATP and mesitylenecarboxylic acid in polyacrylamide gel in the presence of sodium dodecyl sulphate showed that the inhibitor is bound to the beta-subunit of the enzyme. The results suggest that ATP may also bind to the beta-subunit of the adenosine triphosphatase with its triphosphate moiety.

Adenosine Triphosphatases↗

PubMed1989

Extracellular adenosine triphosphate increases cation permeability of chronic lymphocytic leukemic lymphocytes.

Extracellular adenosine triphosphate (ATP) is known to reversibly increase the cation permeability of a variety of freshly isolated and cultured cell types. In this study the effects of extracellular ATP were studied using peripheral blood lymphocytes (PBL) isolated from both normal subjects and from patients with chronic lymphocytic leukemia (CLL). Changes in the permeability to Na+, Rb+, and Li+ ions were measured using conventional isotope and flame photometry techniques. In addition, changes in cytosolic (Ca2+) were fluorimetrically monitored to assess possible changes in net Ca2+ influx. ATP produced a 12-fold increase in 22Na+ influx into CLL cells but only a 3.5-fold increase in this flux in PBL cells. A maximal response was produced by 0.1 mmol/L ATP in the absence of Mg2+, while a twofold molar excess of Mg2+ over ATP abolished the response. ATP had no effect on the passive (ouabain-insensitive) 86Rb+ influx into PBL cells but stimulated this flux by fivefold in the CLL cells. Li+ influx into CLL cells was also stimulated threefold by ATP. Under these same conditions ATP also produced a net increase in total cell Na and a decrease in total cell K in the CLL cells. Exclusion of two normally impermeable dyes, trypan blue and ethidium bromide, was not altered in the ATP-treated CLL cells. Finally, extracellular ATP (3 mmol/L) produced no significant change in the cytosolic (Ca2+) of normal, monocyte-depleted populations of PBL. Conversely, this same concentration of ATP produced a very rapid (complete within 30 seconds) and a significant (an average threefold peak change) increase in the cytosolic (Ca2+) of cell preparations derived from five out of nine CLL patients. In these latter CLL cells, the ATP-induced elevation in cytosolic (Ca2+) appeared to be due to a net increase in Ca2+ influx, since no elevations were observed when the extracellular (Ca2+) was reduced to less than 0.1 mmol/L. These actions of ATP were specific in that equimolar concentrations of other nucleotides were without effect. These data indicate that treatment of CLL lymphocytes with extracellular ATP4 produces large increases in cation permeability. In contrast, there is less or no ATP-induced permeabilization of normal PBL.

Adenosine Triphosphate↗

PubMed1983

Possible source of adenosine triphosphate released from rat myocytes in response to hypoxia and acidosis.

Ventricular cells from adult rats were isolated enzymatically and used as a model system for determining what factors affect the release of adenosine triphosphate (ATP) from myocardial cells. The enzyme systems used to isolate cells were trypsin:collagenase; hyaluronidase:collagenase and dispase:collagenase. Adenosine triphosphate was released in greater amounts in response to hypoxia from cells freed by each of the enzymatic procedures. This occurred while the intracellular concentration of ATP remained constant. Experiments were then performed to determine whether the conditions that occur during myocardial ischaemia or hypoxia altered the release of ATP. Cells suspended in either oxygenated or anoxic buffer at a pH of 6.8 released a significantly lower amount of ATP than cells suspended in either condition at pH 7.4. To test the possibility that ATP was released from nucleotide-protein-Ca2+ complexes located in the sarcolemma, artificial disruption of these structures was carried out. Incubation of oxygenated cells with the chelating agent, ethyleneglycol-bis (B-aminoethyl ether)-N, N-tetraacetic acid (EGTA), stimulated the release of ATP in a hyperbolic relationship while incubation of anoxic cells with ethylenediamine tetraacetate (EDTA) stimulated the release of ATP in such a way that the pattern of release followed a sigmoid response with maximal amounts of ATP, 995 +/- 55 pmol.mg-1 protein, occurring in the presence of 0.1 to 2.0 mmol.litre-1 EDTA. By incubating cells with radioactive EDTA, there was no indication that EDTA entered the cells. No release of ATP above control levels occurred when EDTA was chelated with Ca2+ before being applied to isolated cells. These data suggest that the source of ATP found extracellularly may have been nucleotide-protein-Ca2+ complexes located in the sarcolemma, and further support the role of ATP as a coronary vasodilator during hypoxic conditions.

Adenosine Triphosphate↗

PubMed1989

Selective enhancement of intratumoural blood flow in malignant gliomas: experimental study in rats by intracarotid administration of adenosine or adenosine triphosphate.

We studied the effect of intravenous and intracarotid infusion of adenosine and adenosine triphosphate (ATP) on the regional blood flow of intracerebrally transplanted RG-C6 tumours in rats, using the hydrogen clearance method. The intracarotid administration of adenosine or ATP selectively increased blood flow in the tumour, but did not produce any significant change either in the regional cerebral blood flow of the extratumoural ipsilateral hemisphere or in the ipsilateral hemisphere without tumour. The intracarotid administration of ATP at a dose of 10 micrograms/kg/min produced the most effective increase in the tumour blood flow (+51.5 +/- 16.8%). In contrast, both the intravenous administration of adenosine and that of ATP failed to increase tumour blood flow. These results may possibly indicate that intracarotid administration of the adenosine or ATP might contribute in selectively enhancing the delivery of anti-cancer agents to malignant brain tumours.

Adenosine↗

PubMed2004

Role of macula densa adenosine triphosphate (ATP) in tubuloglomerular feedback.

BACKGROUND: Recent studies have shown that adenosine triphosphate (ATP) is liberated from macula densa cells in response to increased tubular NaCl in vitro. We tested the hypothesis that increased NaCl in the macula densa stimulates the release of ATP, resulting in extracellular formation of adenosine which is involved in signal transmission of the tubuloglomerular feedback response. METHODS: Rabbit afferent arterioles and attached macula densas were simultaneously microperfused in vitro. Tubuloglomerular feedback was induced by increasing macula densa Na/Cl from 11/10 to 81/80 mmol/L and was measured before and after treatment. RESULTS: We first tested whether hydrolysis of ATP is required for tubuloglomerular feedback. When we enhanced conversion of ATP to adenosine by adding hexokinase or apyrase to the bath and arteriole lumen, the tubuloglomerular feedback response was augmented. During the control period, tubuloglomerular feedback decreased arteriole diameter by 2.2 +/- 0.2 microm. In the presence of hexokinase, tubuloglomerular feedback decreased diameter by 3.4 +/- 0.3 microm (N= 8) (P < 0.05, with vs. without hexokinase). In the apyrase group, tubuloglomerular feedback decreased diameter by 2.7 +/- 0.4 microm during the control period. When apyrase was added, tubuloglomerular feedback decreased diameter by 4.7 +/- 0.4 microm (N= 8) (P < 0.05, with vs. without apyrase). When hydrolysis of adenosine monophosphate (AMP) to adenosine was blocked by supplementing the bath with 100 micromol/L alpha,beta-methylene adenosine 5'-diphosphate (MADP), an inhibitor of 5'-nucleotidase, tubuloglomerular feedback response was blocked and diameter remained unchanged. We next studied whether ATP released from the macula densa binds to P(2) receptors and activates the tubuloglomerular feedback response. The P(2) purinergic receptor inhibitor suramin was added to both arteriole lumen and bath. During the control period, tubuloglomerular feedback decreased diameter by 3.7 +/- 0.5 microm. Suramin (100 micromol/L) did not significantly inhibit tubuloglomerular feedback, since in the presence of suramin diameter decreased by 3.8 +/- 0.3 microm (N= 7). Finally, we added the adenosine A(1) receptor inhibitor FK838 to both bath and lumen and found that it completely blocked high NaCl-induced tubuloglomerular feedback. CONCLUSION: We concluded that ATP released from the macula densa is broken down to form AMP in the extracellular space. AMP in turn is degraded by ecto-5'-nucleotidases to adenosine, which mediates signal transmission of the tubuloglomerular feedback response.

5'-Nucleotidase↗

PubMed2006

Energy transfer from adenosine triphosphate.

We suggest a direct molecular mechanism of energy transfer from adenosine triphosphate (ATP) in hydrolysis and phosphorylation reactions, from chemical energy into mechanical energy. Upon hydrolysis of ATP, say bound to a protein, the electrostatic energy of Coulombic repulsion of the ions adenosine diphosphate and phosphate is available to assert a force on a neighboring molecular group in the protein and can do work on that group, or as the ions recede from each without asserting such a force, they gain relative kinetic energy, which, in the absence of dissipative collisions that turn this kinetic energy into heat, can be converted into any other form of energy and work by an impulse, a collision with a neighboring group, without restrictions. Either possibility can be used as a source of activation energy for reactions, as a source of energy to surmount energy barriers in conformational changes, and as a source of work to be done, as in muscle. In some systems where the Gibbs free energy change is fully utilized, all of this energy is turned into mechanical energy, and we suggest a similar mechanism. From the literature we cite some experimental evidence and several quotations indicative of the possibility of our suggestion.

Actins↗

PubMed2003

Propofol suppresses macrophage functions and modulates mitochondrial membrane potential and cellular adenosine triphosphate synthesis.

BACKGROUND: Propofol is an intravenous anesthetic agent that may impair host defense system. The aim of this study was to evaluate the effects of propofol on macrophage functions and its possible mechanism. METHODS: Mouse macrophage-like Raw 264.7 cells were exposed to propofol, at 3, 30 (a clinically relevant concentration), and 300 microm. Cell viability, lactate dehydrogenase, and cell cycle were analyzed to determine the cellular toxicity of propofol to macrophages. After administration of propofol, chemotactic, phagocytic, and oxidative ability and interferon-gamma mRNA production were carried out to validate the potential effects of propofol on macrophage functions. Mitochondrial membrane potential and cellular adenosine triphosphate levels were also analyzed to evaluate the role of mitochondria in propofol-induced macrophage dysfunction. RESULTS: Exposure of macrophages to 3 and 30 microm propofol did not affect cell viability. When the administered concentration reached 300 microm, propofol would increase lactate dehydrogenase release, cause arrest of cell cycle in G1/S phase, and lead to cell death. In the 1-h-treated macrophages, propofol significantly reduced macrophage functions of chemotactic and oxidative ability in a concentration-dependent manner. However, the suppressive effects were partially or completely reversed after 6 and 24 h. Propofol could reduce phagocytic activities of macrophages in concentration- and time-dependent manners. Exposure of macrophages to lipopolysaccharide induced the mRNA of interferon-gamma, but the induction was significantly blocked by propofol. Propofol concentration-dependently decreased the membrane potential of macrophage mitochondria, but the effects were descended with time. The levels of cellular adenosine triphosphate in macrophages were also reduced by propofol. CONCLUSIONS: A clinically relevant concentration of propofol can suppress macrophage functions, possibly through inhibiting their mitochondrial membrane potential and adenosine triphosphate synthesis instead of direct cellular toxicity.

Actins↗

PubMed2003

Mechanism of syncope in patients with positive adenosine triphosphate tests.

OBJECTIVES: We prospectively evaluated the mechanism of syncope in patients with positive adenosine triphosphate (ATP) tests (defined as the induction of atrioventricular [AV] block with a ventricular pause >/=6 s after an intravenous bolus of 20 mg ATP). BACKGROUND: Patients with unexplained syncope tend to have more positive ATP tests results than those without syncope. METHODS: An implantable loop recorder (ILR) was inserted in 36 ATP-positive patients (69 +/- 10 years; 22 women; median of 6 syncopal episodes); 15 of them also had a positive response to tilt testing. RESULTS: During the follow-up of 18 +/- 9 months, 18 patients (50%) had syncopal recurrence and 16 (44%) had an electrocardiographically documented episode: AV block (n = 3: paroxysmal in 2 and permanent in 1), AV block followed by sinus arrest (n = 1), sinus arrest (n = 5), sinus bradycardia <40 beats/min (n = 2), normal sinus rhythm (n = 2), sinus tachycardia (n = 1), rapid atrial fibrillation (n = 1), and ectopic atrial tachycardia (n = 1). Bradycardia was documented in a total of 11 cases (69%), and a long ventricular pause (4 to 29 s) was present in eight cases (50%). All three patients with ILR-documented AV block had previously had a negative tilt test, whereas seven of eight with ILR-documented sinus bradycardia or sinus arrest had previously had a positive tilt test. CONCLUSIONS: In patients with adenosine-sensitive syncope, the mechanism of syncope is heterogeneous, although bradycardia is the most frequent finding. Adenosine triphosphate-induced AV block predicts AV block as the mechanism of spontaneous syncope in only a few tilt-negative patients.

Adenosine Triphosphate↗