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At least 685 records · Page 38Linked to original sources
PubMed1969

Identification of adenosine triphosphate in human plasma and the concentration in the venous effluent of forearm muscles before, during and after sustained contractions.

1. When diluted human plasma is perfused through a frog heart, a marked augmentation of the heartbeat is produced which is very similar in action to that of low concentrations of adenosine triphosphate (ATP) on the heart.2. It was established that the substance in the plasma responsible for the heart stimulation was ATP. The following tests were used: (a) the diluted plasma emitted light from firefly lantern extract characteristic of the light signal produced by a solution of ATP; (b) the stimulatory effect on the frog heart and luminescent effect upon the firefly extract were abolished by incubation of the plasma solution with the enzyme apyrase, which converts ATP to adenosine monophosphate (AMP); AMP does not stimulate the heart or cause light to be emitted from firefly extract; (c) the stimulatory substance in the plasma was eluted through a column of Sephadex G-25 in the same pattern as ATP; and (d) simultaneous assay of plasma solutions on frog heart and firefly extract produced the same quantitative result as that produced by a solution of ATP.3. The amount of ATP in plasma from the venous blood of resting subjects ranged from 0.19 to 0.95 mug/ml. (mean 0.63 mug/ml., S.D. +/- 0.25); up to half of the ATP detected could be attributed to blood platelet damage. Simultaneous arterial and venous samples of blood from four subjects at rest had mean concentrations of 0.19 mug/ml. (0.07-0.26 mug/ml.) and 0.70 mug/ml. (0.57-0.84 mug/ml.) respectively.4. The concentration of ATP in the venous effluent from exercising forearm muscles was measured. The venous concentration consistently increased over the resting values in response to exercise while in one subject little change occurred in the arterial blood concentration during the exercise. It was concluded that the ATP was added to the blood in its passage through the muscle bed.5. The origin of the ATP, including erythrocytes, blood platelets and active skeletal muscle, is discussed.

Adenine Nucleotides↗
PubMed2006

Extracellular adenosine triphosphate protects oxidative stress-induced increase of p21(WAF1/Cip1) and p27(Kip1) expression in primary cultured renal proximal tubule cells: role of PI3K and Akt signaling.

Oxidative stress, the result of cellular production of reactive oxygen species (ROS), has been implicated in causing many renal diseases. Adenosine triphosphate (ATP) is an important extracellular signal in the regulation of many intracellular processes in normal tubular cells as well as in the pathogenesis of cell injury. This study investigated the effect of ATP on H(2)O(2)-induced increase of cyclin kinase inhibitors (CKI) expression and its related signal molecules in primary cultured renal proximal tubule cells (PTCs). H(2)O(2) inhibited DNA synthesis in a concentration- (>50 microM) and time-dependent manner (>2 h), as determined by thymidine and BrdU incorporation, and by increase in the p21(WAF/Cip1) and p27(Kip1) expression levels. In contrast, ATP increased the level of thymidine, BrdU incorporation (>10(-5) M), and decreased the p21(WAF/Cip1) and p27(Kip1) expression levels, suggesting that ATP has a protective effect against H(2)O(2)-induced oxidative damage. Suramin, reactive blue 2 (RB-2), MRS 2159, and MRS 2179 did block the reversing effect of ATP. In addition, AMP-CPP or 2-methylthio-ATP blocked H(2)O(2)-induced inhibition of DNA synthesis, suggesting all these P2 purinoceptors may be potentially involved. ATP-induced stimulation of DNA synthesis was blocked by phosphatidylinositol 3-kinase (PI3K) and Akt inhibitors. These results suggest the involvement of P2 purinoceptors-mediated PI3K/Akt signal pathway in the protective effect of ATP against H(2)O(2)-induced oxidative damage. Indeed, pre-treatment with PI3K or Akt inhibitors did not protect H(2)O(2)-induced lipid peroxide (LPO) production and inhibition of thymidine incorporation. In conclusion, ATP, in part, blocked H(2)O(2)-induced increase of p21(WAF1/Cip1) and p27(Kip1) expression through PI3K and Akt signal pathway in renal PTCs.

Adenosine Triphosphate↗
PubMed1988

Characterization of the myosin adenosine triphosphate (M.ATP) crossbridge in rabbit and frog skeletal muscle fibers.

In the presence of ATP and absence of Ca2+, muscle crossbridges have either MgATP or MgADP.Pi bound at the active site (S. B. Marston and R. T. Tregear, Nature [Lond.], 235:22:1972). The behavior of these myosin adenosine triphosphate (M.ATP) crossbridges, both in relaxed skinned rabbit psoas and frog semitendinosus fibers, was analyzed. At very low ionic strength, T = 5 degrees C, mu = 20 mM, these crossbridges spend a large fraction of the time attached to actin. In rabbit, the attachment rate constants at low salt are 10(4) - 10(5) s-1, and the detachment rate constants are approximately 10(4) s-1. When ionic strength is increased up to physiological values by addition of 140 mM potassium propionate, the major effect is a weakening of the crossbridge binding constant approximately 30-40-fold. This effect occurs because of a large decrease, approximately 100-fold, in the crossbridge attachment rate constants. The detachment rate constants decrease only 2-3-fold. The effect of ionic strength on crossbridge binding in the fiber is very similar to the effect of ionic strength on the binding of myosin subfragment-1 to unregulated actin in solution. Thus, the effect of increasing ionic strength in fibers appears to be a direct effect on crossbridge binding rather than an effect on troponin-tropomyosin. The finding that crossbridges with ATP bound at the active site can and do attach to actin over a wide range of ionic strengths strongly suggests that troponin-tropomyosin keeps a muscle relaxed by blocking a step subsequent to crossbridge attachment. Thus, rather than troponin-tropomyosin serving to keep a muscle relaxed by inhibiting attachment, it seems quite possible that the main way in which troponin-tropomyosin regulates muscle activity is by preventing the weakly-binding relaxed crossbridges from going on through the crossbridge cycle into more strongly-binding states.

Adenosine Triphosphate↗
PubMed1991

Correlation between high adenosine triphosphate tissue concentration and good posttransplant outcome for the canine pancreas graft after preservation by the two-layer cold storage method.

Assessment of viability of a pancreas graft during preservation is very important to avoid transplantation of a nonfunctioning allograft. In the present report the correlation between adenosine triphosphate tissue concentration at the end of cold preservation by the two-layer method and viability a of canine pancreas graft following transplantation was studied. After preservation by an original two-layer (Euro-Collins' solution/perfluorochemical) method (group 1) and a modified two-layer (University of Wisconsin solution/PFC) method (group 2) for 24, 48, 72, 96, and 120 hr (subgroups A, B, C, D, and E), the tissue concentration of ATP was determined using high-performance liquid chromatography, and the viability of the pancreas graft was tested in the canine model of segmental pancreas autotransplantation. Maintenance of normoglycemia for at least five days after transplantation was considered to indicate a viable pancreas graft. In group 1, functional success rates were A: 5/5, (100%), B: 4/4 (100%), C: 4/4, (100%), and D: 0/4 (0%), respectively. The ATP tissue concentrations were 7.47 +/- 0.47 (n = 5), 7.91 +/- 1.21 (n = 4), 8.29 +/- 0.21 (n = 4), and 4.94 +/- 1.11 (n = 4) mumol/g dry weight in groups 1A, 1B, 1C, and 1D, respectively. There was a statistically significant difference between viable groups (groups 1A, 1B, and 1C, 7.86 +/- 0.77 mumol/g dry weight [n = 13]) and the nonviable group (group D, 4.94 +/- 1.11 mumol/g dry weight (n = 4) (P less than 0.01). On the other hand, the functional success rates were 3/3 (100%), 3/3 (100%), 3/3 (100%), 5/7 (71%), and 0/3 (0%) in groups 2A, 2B, 2C, 2D, and 2E, respectively. Two of seven dogs died of causes related to the grafts (pancreatitis and thrombosis). The ATP tissue concentrations were 8.53 +/- 1.45 (n = 3), 9.64 +/- 1.77 (n = 3), 13.81 +/- 2.09 (n = 3), and 12.49 +/- 2.52 (n = 5) mumol/g dry weight in groups 2A, 2B, and 2C and in viable grafts in group 2D, respectively, but the ATP tissue concentration of nonviable grafts in group 2D and group E were 3.51 +/- 0.81 (n = 2) and 3.98 +/- 1.34 (n = 3) mumol/g dry weight, respectively. There was a statistically significant difference between viable groups (groups 2A, 2B, 2C and viable grafts in group 2D, 11.03 +/- 2.72 mumol/g dry weight [n = 14]) and nonviable groups (group E and nonviable grafts in group 2D, 3.79 +/- 1.06 mumol/g dry weight [n = 5]) (P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1987

Effects of adenosine triphosphate depletion in the isolated perfused rat kidney.

Glycerol or fructose (40 mM) was added to the control perfusate and renal function was observed in the isolated perfused rat kidney during nonischemic perfusions or perfusions following 30 min of clamp ischemia. Addition of glycerol or fructose resulted in lowering adenosine triphosphate (ATP) levels to 62 and 35%, respectively, of levels achieved with control perfusate under nonischemic conditions (p less than 0.01). Total adenine nucleotides (TAN) were also lowered to 67% with glycerol and 61% with fructose of control values under nonischemic conditions (p less than 0.05). However, physiologic parameters of renal plasma flow and inulin clearance were essentially unaffected by either glycerol or fructose. Following ischemia, glycerol and fructose reduced ATP levels to 51 and 37% and TAN levels to 67 and 65%, respectively, of values seen with control perfusate. However, recovery of renal plasma flow and inulin clearance were uneffected by the addition of either glycerol or fructose. Thus, a 33-65% reduction in renal tissue ATP by glycerol or fructose does not appear to have a deleterious effect on organ function in the basal state or during recovery from an ischemic insult in the isolated perfused rat kidney.

Adenine Nucleotides↗
PubMed2005

Effect of adenosine triphosphate in renal ischemic injury: involvement of NF-kappaB.

Renal ischemic/reperfusion injury in vivo results in a significant increase of acute renal failure (ARF) and death. Nevertheless, there are many limitations in using in vivo models of renal ischemic injury to elucidate the detailed mechanisms of renal injury. Adenosine triphosphate (ATP), an extracellular signal, has been shown to be an important factor in regulation of epithelial cell function. Thus, the present study was performed to establish in vitro ischemic model using primary cultured rabbit renal proximal tubule cells (PTCs) and to examine the effect of ATP in this model. We established an in vitro model of ischemic injury, causing severe depletion of intracellular ATP by using the combination of a mitochondrial respiration inhibitor (antimycin A), non-metabolizable glucose analog (2-deoxyglucose), and calcium ionophore (A23187) in PTCs. Indeed, this ischemic injury significantly increased LDH release, a marker of structural damage, and ATP blocked ischemic injury-induced LDH release. 2-Methylthio-ATP and ATP-gamma-S (P2Y purinoceptor agonists) also blocked ischemic injury-induced LDH release, whereas AMP-CPP (P2X purinoceptor agonist) did not block it. In experiments to examine the relationship between ischemic injury and NF-kappaB activation, ischemic injury increased NF-kappaB translocation, DNA binding activity, and CAT activity. On the other hand, ATP, ATP-gamma-S, or 2-methylthio-ATP protected ischemic injury-induced NF-kappaB activation. These results suggest that the protective effect of ATP on ischemic injury is, in part, related to inhibition of NF-kappaB activation via P2Y receptor in PTCs.

Adenosine Triphosphate↗
PubMed1989

Stimulation-dependent release of adenosine triphosphate from hippocampal slices.

Schaffer collaterals of rat and mouse hippocampal slices were stimulated with bursts of pulses (300 Hz for 50 ms, 2-s intervals) for 30-s which caused a stable increase in the size of the population spike known as long-term potentiation. The release of adenosine triphosphate (ATP) was measured with a luciferase-luciferine system and the light emitted was recorded with a photomultiplier placed beneath a modified slice chamber. ATP release was observed shortly after the start of stimulation and was quantified by comparison with the response of standard solutions of ATP. No ATP release was observed in a Ca2+ free solution or after low frequency stimulation (1 Hz). Glutamate (2 mM), applied without electrical stimulation, did not evoke ATP release. Also, the glutamate receptor blocker, kynurenic acid (10 mM), did not block ATP release. It is concluded that ATP is released from electrically stimulated hippocampal slices from presynaptic nerve terminals in a calcium-dependent fashion and may play a role in the modulation of synaptic efficiency.

Action Potentials↗
PubMed1996

Effects of oxyhemoglobin on local and propagated vasodilatory responses induced by adenosine, adenosine diphosphate, and adenosine triphosphate in rat cerebral arterioles.

After subarachnoid hemorrhage (SAH), cerebral arteries display impaired vasomotor control, resulting in decreased regional cerebral blood flow. Recently, propagation of vasomotor responses has been recognized as an important regulatory mechanism in microcirculation. In this study, the authors tested the hypothesis that oxyhemoglobin (OxyHb) inhibits the vasodilatory effect of chemical mediators such as adenosine and adenine nucleotides at a local and/or propagated site. Penetrating intracerebral arterioles were surgically isolated from the middle cerebral arteries of rat brains, cannulated, and observed videomicroscopically in an organ bath under an inverted microscope. The effects of 10(-5) M OxyHb on vasoactive responses to adenosine, adenosine diphosphate (ADP), and adenosine triphosphate (ATP) were examined. The drugs were extraluminally applied either to the bath (10(-10)-10(-3) M) or, using pressure microejection (pipette concentration 10(-2) M), locally. The ATP and ADP initially constricted and then significantly dilated the vessels after both extraluminal application and microapplication. Furthermore, local microstimulation by these drugs produced conducted vasodilation. Adenosine elicited significant vasodilation after both extraluminal and local stimulation. Again, conducted vasodilation was observed. The vasomotor responses that were induced by a maximum local stimulation corresponded in magnitude to those observed at bath concentrations of 10(-5) to 10(-4) M of the same drug. Pretreatment with OxyHb constricted arterioles to an average of 87% of control and blunted extraluminally induced dilation at low concentrations (10(-10)-10(-8)) of ATP and ADP, but did not affect vasodilation induced by 10(-4) M or greater concentrations of ATP, ADP, or adenosine. Although the local response to local microstimulation was unaltered, propagated vasodilation as a response to ATP, ADP, and adenosine was significantly attenuated by OxyHb. These findings indicate that vasodilatory propagation plays an important role in the regulation of brain microcirculation and that its impairment by OxyHb could, in part, explain the cerebral hypoperfusion that is observed after SAH.

Adenosine↗
PubMed1988

Comparison of cell death and adenosine triphosphate content as indicators of acute toxicity in vitro.

1. Anchorage-independent LS cells, derived from L929 mouse fibroblasts, were used as an in vitro alternative to animals for the assessment of acute toxicity. The two end points were cell death, indicated by fluorescein diacetate and ethidium bromide, and intracellular adenosine triphosphate (ATP) content. 2. Concentrations of 20 test compounds which produced a 50% decrease in the ATP contents of control cells (ATP50) ranged from 17 micrograms ml-1 for diethylstilboestrol to 7.0 mg ml-1 for sodium chloride. 3. The concentrations which caused 50% cell death ranged from 16 micrograms ml-1 for diethylstilboestrol to 8.0 mg ml-1 for paracetamol. 4. There was a good numerical correlation (r = 0.99) between the ranks of ATP50 and CD50 end-points, there being only minor changes in order between the ranks. 5. The slopes of the dose-response plots for individual chemicals were markedly different.

Acetaminophen↗
PubMed1995

Prostanoid secretion by rat hepatic sinusoidal endothelial cells and its regulation by exogenous adenosine triphosphate.

We investigated the secretory profiles of prostanoids in two types of nonparenchymal cell from the rat liver, sinusoidal endothelial cells and Kupffer cells, in primary culture both under basal conditions and after stimulation with adenine nucleotides. Prostaglandin (PG) E2 was the main prostanoid secreted by both types of hepatic nonparenchymal cell in the basal and adenosine triphosphate (ATP)-stimulated states. Time- and concentration-dependent effects of ATP-mediated PGE2 secretion were noted in sinusoidal endothelial cells, whereas the profile of the relative potencies of individual nucleotides was consistent with the presence of P2y and P1 purinergic receptors. In Kupffer cells, the regulation of prostanoid secretion by adenine nucleotides was essentially the same as that in sinusoidal endothelial cells except that adenosine did not stimulate prostanoid secretion and that prostanoid secretion differed somewhat; Kupffer cells secreted relatively more PGF2 alpha and less 6-keto-PGF1 alpha than sinusoidal endothelial cells in the presence of ATP, suggesting the presence of only P2y receptors. In summary, PGE2 is the main prostanoid secreted by hepatic nonparenchymal cells and its secretion may be stimulated by adenine nucleotides and adenosine.

Adenine Nucleotides↗
PubMed1973

Action of adenosine triphosphate on endplate potentials recorded from muscle fibres of the rat-diaphragm and frog sartorius.

Evoked and spontaneous endplate potentials (e.p.ps) were recorded with intracellular electrodes from fibres of the rat diaphragm and the frog sartorius muscle. The amplitudes of the evoked e.p.ps were reduced to about one-half their control values in the presence of 0.1 mm and 0.2 mm of adenosine triphosphate (ATP). The amplitude of the spontaneous endplate potentials (miniature e.p.ps) was unaffected by ATP but their frequency was reduced.

Adenosine Triphosphate↗
PubMed1996

The diadenosine polyphosphates Ap3A and Ap4A and adenosine triphosphate interact with granulocyte-macrophage colony-stimulating factor to delay neutrophil apoptosis: implications for neutrophil: platelet interactions during inflammation.

Incubation of neutrophils with cytokines such as granulocyte macrophage colony-stimulating factor (GM-CSF) delays their loss of function and changes in cellular morphology that are characteristic of apoptosis. Adenosine triphosphate (ATP) and the diadenosine polyphosphates Ap4A and AP3A were almost as effective as GM-CSF in delaying neutrophil apoptosis. The nucleotides could thus preserve cellular morphology, protect against chromatin fragmentation, and preserve functions such as NADPH oxidase activity and expression of CD16. Moreover, addition of ATP, AP3A and AP4A together with GM-CSF resulted in more pronounced protection from apoptosis than was observed during incubation with either the cytokine or the nucleotides alone. Because ATP, Ap3A, and AP4A may be secreted from activated platelets, these observations suggest that platelet-derived products, perhaps acting in combination with endothelial-derived or immune cell-derived cytokines, can regulate neutrophil function during certain types of inflammation.

Adenosine Triphosphate↗
PubMed2001

Adenosine and adenosine triphosphate modulate the substrate binding affinity of glucose transporter GLUT1 in vitro.

Evidence indicates that a large portion of the facilitative glucose transporter isoform GLUT1 in certain animal cells is kept inactive and activated in response to acute metabolic stresses. A reversible interaction of a certain inhibitor molecule with GLUT1 protein has been implicated in this process. In an effort to identify this putative GLUT1 inhibitor molecule, we studied here the effects of adenosine and adenosine triphosphate (ATP) on the binding of D-glucose to GLUT1 by assessing their abilities to displace cytochalasin B (CB), using purified GLUT1 in vesicles. At pH 7.4, adenosine competitively inhibited CB binding to GLUT1 and also reduced the substrate binding affinity by more than an order of magnitude, both with an apparent dissociation constant (K(D)) of 3.0 mM. ATP had no effect on CB and D-glucose binding to GLUT1, but reduced adenosine binding affinity to GLUT1 by 2-fold with a K(D) of 30 mM. At pH 3.6, however, ATP inhibited the CB binding nearly competitively, and increased the substrate binding affinity by 4--5-fold, both with an apparent K(D) of 1.22 mM. These findings clearly demonstrate that adenosine and ATP interact with GLUT1 in vitro and modulate its substrate binding affinity. They also suggest that adenosine and ATP may regulate GLUT1 intrinsic activity in certain cells where adenosine reduces the substrate-binding affinity while ATP increases the substrate-binding affinity by interfering with the adenosine effect and/or by enhancing the substrate-binding affinity at an acidic compartment.

Adenosine↗
PubMed1988

Adenosine triphosphate can maintain multipotent haemopoietic stem cells in the absence of interleukin 3 via a membrane permeabilization mechanism.

The survival, proliferation and development of haemopoietic stem cells in vitro requires the presence of specific growth factors such as Interleukin 3, in the absence of these growth factors the cells die very rapidly (8-48 hours). Adenosine triphosphate can maintain an Interleukin 3 dependent stem cell line in the absence of this growth factor for periods up to and beyond 48 hours. This effect of ATP is mediated by an increase in plasma membrane permeability. ATP mediated survival will be an important tool in studying both Interleukin 3 dependence of stem cells and also in the study of stem cell differentiation.

Adenosine Triphosphate↗
PubMed1997

Intracellular adenosine triphosphate (ATP) concentration: a switch in the decision between apoptosis and necrosis.

Apoptosis and necrosis are considered conceptually and morphologically distinct forms of cell death. Here, we report that demise of human T cells caused by two classic apoptotic triggers (staurosporin and CD95 stimulation) changed from apoptosis to necrosis, when cells were preemptied of adenosine triphosphate (ATP). Nuclear condensation and DNA fragmentation did not occur in cells predepleted of ATP and treated with either of the two inducers, although the kinetics of cell death were unchanged. Selective and graded repletion of the extramitochondrial ATP/pool with glucose prevented necrosis and restored the ability of the cells to undergo apoptosis. Pulsed ATP/depletion/repletion experiments also showed that ATP generation either by glycolysis or by mitochondria was required for the active execution of the final phase of apoptosis, which involves nuclear condensation and DNA degradation.

Adenosine Triphosphate↗
PubMed1980

Oxygen consumption and cellular ion transport: evidence for adenosine triphosphate to O2 ratio near 6 in intact cell.

Oxygen (O2) consumption and net K+ uptake were measured simultaneously upon reintroduction of K+ into a K+-depleted suspension of renal tubules. The K+/O2 stoichiometries of 11.8 +/- 0.2 and 8.4 +/- 0.6 were obtained for reduced nicotinamide adenine dinucleotide- and flavoprotein-linked substrates, respectively. These values complement classical K+ to adenosine triphosphate (ATP) and ATP/O2 stoichiometries, thereby demonstrating a remarkably efficient coupling between the processes of Na+- and K+-dependent adenosinetriphosphatase-mediated ion transport and oxidative phosphorylation within the intact cell.

Adenosine Triphosphate↗
PubMed1998

Slow ventricular tachycardia located in the epicardium of the left ventricular base and characterized by effects of adenosine triphosphate, nicorandil and verapamil.

A 31-year-old male with slow ventricular tachycardia (VT) developed a nonsustained VT with prolongation of the JT intervals after injection of contrast medium and saline into the marginal vein of the coronary sinus. The earliest activation site of the VT existed in the epicardium of the left ventricular base. Adenosine triphosphate prevented induction of VT and prolongation of JT intervals. Ventricular premature contractions showing the same morphology as the VT were also inhibited by nicorandil and verapamil. The mechanism of the VT was suggested to be abnormal automaticity due to an increase in the Ca++ current into cells after prolongation of the action potential duration induced by hypothermia.

Adenosine Triphosphate↗