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PubMed1976

Effects of Listeria monocytogenes and its components on adenosine triphosphate concentrations in mice.

The effects of Listeria monocytogenes and its components on adenosine triphosphate (ATP) concentrations in mice were examined by in vitro and in vivo techniques. White female mice were intraperitoneally injected with L monocytogenes strain 9-125 and its components, and certain tissues of mice were exposed to the various listerial components in vitro, and the ATP concentrations in these tissues were measured. Results of in vivo experiments indicated that live listerial cells and certain components (hemolysin, cell wall, and cytoplasm) decreased the ATP concentrations in some tissues of the mice, whereas other components (peptidoglycan and endotoxin-like material) did not have any effects on ATP concentrations. Although hemolysin from L monocytogenes decreased the tissue ATP concentrations in vitro, other listerial components did not effect any of the exposed tissues. The data indicated some impairment of host energy metabolism occurred in mice exposed to L monocytogenes or to its components or to both.

Adenosine Triphosphate↗

PubMed1975

Relationship between coronary flow and adenosine triphosphate production from glycolysis and oxidative metabolism.

The relationship between coronary flow and adenosine triphosphate ATP production was determined in isolated rat hearts and in situ pigs hearts. The major source of ATP in ischemic hearts was oxidative phosphorylation. Oxidation of glucose accounted for most of the residual oxygen consumption in ischemic hearts when the concentration of fatty acids was low, but at 1.2 mM palmitate fatty acids were oxidized in preference to carbohydrate, as in aerobic hearts. The rates of ATP production from both glycolysis and oxidative metabolism were decreased in proportion to the reduction in coronary flow in oxygen-deficient hearts. Glycolysis was reduced to below aerobic rates when coronary flow was about 0.5 ml/min/g tissue in both rat hearts perfused with bicarbonate buffer and blood-perfused pig hearts. Tissue level of high energy phosphates reflected the rates of ATP production and declined in proportion to the reduction in coronary flow. In addition, tissue lactate and H+ accumulated in proportion to the restriction in flow.

Adenosine Triphosphate↗

PubMed1987

Intracellular adenosine triphosphate as a measure of human tumor cell viability and drug modulated growth.

Adenosine triphosphate is the primary energy unit for cells, and levels of this compound offer a potential marker for cell viability and growth. The availability of a bioluminescence assay allows for a rapid, sensitive, and reproducible measurement of ATP. A method is described for the quantification of intracellular ATP levels in human cancer cells. ATP levels were linearly related to the number of viable cells and increased with time in human cancer cell line cultures correlating with growth kinetics. The effect of 5-fluorouracil, doxorubicin, methotrexate, cytosine arabinoside, nitrogen mustard, melphalan, vinblastine, and cisplatin on the growth of human cancer cell lines was studied utilizing ATP levels. ATP levels and colony formation in agar of drug-exposed cells were compared. Overall there was a significant correlation between drug effects on colony formation and ATP levels. The ATP assay is rapid, simple, reproducible, and a relatively inexpensive method of quantifying drug effects on malignant cells. This makes it a potentially useful method for screening new anticancer drugs in human cancer cell lines.

Adenosine Triphosphate↗

PubMed1977

Transient phase of adenosine triphosphate hydrolysis by myosin, heavy meromyosin, and subfragment 1.

The transient phase of adenosine triphosphate (ATP) hydrolysis (early burst) was investigated for myosin, heavy meromyosin (HMM), and subfragment 1 (S-1) over a range of temperatures and pH's. The burst size at pH 8,20 degrees C, is 0.8-0.85, based on steady-state and transient measurements. The equilibrium constant for the enzyme-substrate to enzyme-product transition is 0.85 +/- 0.05. It is concluded that both myosin heads undergo the rapid hydrolysis step and that there are no significant differences for S-1 vs. HMM or myosin. The transient data are fitted reasonably well by a single rate process, but available evidence is consistent with some heterogeneity and a range of rate constants differing by a factor of two. At pH 6.9 and 3 degrees C, the burst size is 0.5 and the hydrolysis is slower than the configuration change measured by fluorescence. The results are consistent with the kinetic scheme (see article). The lower burst at low temperature and pH can be partly explained by a reduction in the equilibrium constant, K3, and ATP can be synthesized on the enzyme by a pH-temperature jump.

Adenosine Triphosphatases↗

PubMed1977

Mechanism of early "pump" failure of the ischemic heart: possible role of adenosine triphosphate depletion and inorganic phosphate accumulation.

A marked reduction in oxygen tension and adenosine triphosphate (ATP) content accompanies the early "pump" failure of the ischemic heart. However, it appears to be unlikely that decreased ATP supplies for energy-consuming reactions in the myocardial cell cause the observed decrease in myocardial contractility because of the high ATP-affinity of the substrate-binding sites of known energy-consuming reactions in the heart. Furthermore, lack of chemical energy for the contractile proteins and known ion pumps would tend to promote rigor and not a decrease in contractility. Recent evidence suggests that ATP at concentrations greater than those needed to saturate the substrate-binding sites of energy-consuming reactions can exert modulatory effects on ion fluxes. These modulatory effects of ATP could allow a less severe decrease in ATP concentration to inhibit both calcium entry into the myocardial cell and calcium efflux from the sarcoplasmic reticulum. In addition, the large amounts of phosphate liberated from phosphocreatine and ATP could, by causing formation of insoluble calcium-phosphate precipitates, trap calcium in the sarcoplasmic reticulum and mitochondria in the ischemic myocardium. These proposed explanations for the early "pump" failure in the ischemic heart, together with other theories such as intracell acidosis, appear to warrant further study.

Adenosine Diphosphate↗

PubMed1996

Changes in Na,K-adenosine triphosphatase (ATPase) concentration and Na,K-ATPase-dependent adenosine triphosphate turnover in human erythrocytes in diabetes.

The concentration of Na,K-adenosine triphosphatase (ATPase) and Na,K-ATPase-dependent adenosine triphosphate (ATP) turnover was measured in fasting blood samples of 20 subjects with insulin-dependent diabetes mellitus (IDDM), 22 subjects with non-insulin-dependent diabetes mellitus (NIDDM), and 20 nondiabetic subjects. [3H]ouabain binding was used to determine Na,K-ATPase concentration. There were 471 +/- 70 (mean +/- SD) ouabain binding sites per erythrocyte, normally distributed in the nondiabetic subjects. The number of ouabain sites per cell was lognormally distributed in the two populations of diabetic subjects. The mean of lognormal distributions of ouabain sites per cell was significantly lower in the IDDM group. The mean of the lognormal distribution for the NIDDM group was not significantly different from that of the nondiabetic subjects. Na,K-ATPase-dependent ATP turnover (molar activity) was 9,580 +/- 742 mol/mol minute (mean +/- SD) normally distributed in the nondiabetic population. A lognormal distribution was observed in the diabetic population. Means of the lognormal distributions were significantly different: 3.98 +/- 0.05 for the nondiabetic population and 3.13 +/- 0.48 for both diabetic populations. Changes in the concentration of Na,K-ATPase (ouabain sites per cell) and Na,K-ATPase-dependent ATP turnover did not correlate with hemoglobin A1C (HbA1C) or with blood glucose. This would suggest that elevated glucose concentrations do not directly cause decreased Na,K-ATPase function in the diabetic erythrocyte.

Adenosine Triphosphate↗

PubMed2005

Comparison of myocardial blood flow induced by adenosine triphosphate and dipyridamole in patients with coronary artery disease.

Myocardial perfusion imaging with adenosine triphosphate (ATP) has been used increasingly to diagnose coronary artery disease (CAD) and assess risk for this disease. This study compared absolute myocardial blood flow (MBF) and myocardial flow reserve index (MFR) with ATP and dipyridamole (DIP) in patients with CAD. MBF was quantified by 15O-H2O PET in 21 patients with CAD (17 male, 4 female), aged 55 to 81 years. MBF was measured at rest, during intravenous injection of ATP (0.16 mg/kg/min), and again after DIP infusion (0.56 mg/kg). Regions of interest were drawn in nonischemic and ischemic segments based on findings from thallium-201 (201T1) scintigraphy and coronary angiography (CAG). Absolute MBF values and indexes of MFR were calculated in nonischemic and ischemic segments. Intravenous injection of ATP and DIP significantly increased MBF in nonischemic (2.4 +/- 0.9 and 2.1 +/- 0.8 ml/g/min, respectively; p < 0.01, for both) and in ischemic segments (1.3 +/- 0.4 and 1.5 +/- 0.4 ml/g/min, respectively; p < 0.01, for both). There was a significant difference in MBF values between ATP and DIP in nonischemic segments (p < 0.05), which was not observed in ischemic segments. In nonischemic segments, ATP produced higher MFR than DIP (2.1 +/- 0.8 and 1.8 +/- 0.7, respectively; p < 0.05), while no significant difference was observed in ischemic segments (1.5 +/- 0.6 and 1.7 +/- 0.3, respectively). ATP produced a greater hyperemia than DIP between the ischemic and nonischemic myocardium in patients with CAD. ATP is as effective as DIP for the diagnosis of CAD.

Adenosine Triphosphate↗

PubMed1997

Effects of intracoronary adenosine triphosphate on coronary flow velocity dynamics in children.

To assess the usefulness of adenosine triphosphate (ATP) as an alternative agent for functional determination of coronary circulation in children and to reveal the dose-response kinetics of intracoronary ATP, systemic hemodynamics and spectral coronary flow velocity dynamics using Doppler guide wire were measured during hyperemic responses to an intracoronary bolus injection of ATP (0.01 microgram/kg, 0.1 microgram/kg and 1.0 microgram/kg) in consecutive 40 Kawasaki disease patients (age: 8.4 +/- 5.1 years, 30 boys and 10 girls) without angiographic coronary lesions. ATP did not produce any significant change in heart rate, systolic blood pressure and mean blood pressure, but mildly decreased diastolic blood pressure. The coronary flow reserve (CFR) calculated as a ratio of hyperemic to basal averaged peak velocity (APV) for ATP was 2.05 +/- 0.31, 2.26 +/- 0.38 and 2.50 +/- 0.51 in LAD, and 2.24 +/- 0.28, 2.44 +/- 0.41 and 2.60 +/- 0.47 in RCA, respectively, for each of the three doses. There was no statistical significance between the mean values of CFR in LAD with ATP (1.0 microgram/kg: 2.39 +/- 0.16) and papaverine (0.15 microgram/kg: 2.43 +/- 0.16) in six patients without angiographic coronary lesions. The maximal coronary hyperemia was reached rapidly after intracoronary bolus injection of ATP in all doses (10, 10-15 and 15-20 seconds in both LAD and RCA, respectively, for each of the three doses). The time required for APV to return to basal levels (< T10%) increased with the dose of ATP (30, 55 and 110 seconds in LAD and 35, 45 and 100 seconds in RCA, respectively, for each of the three doses). Three patients (3/40: 7.5%) developed transient (< 5 seconds) asymptomatic second degree atrioventricular block, but no patient had clinically significant arrhythmias. The change ratio in QTc interval after ATP injection was 1.96 +/- 1.87% (not significant). In addition, an intracoronary injection of ATP did not increase the absolute angiographic coronary luminal diameter. This study indicates that ATP is a safe alternative agent for pharmacological induction of coronary hyperemia for evaluation of coronary stenotic lesions and for the study of coronary circulation and coronary flow reserve in children.

Adenosine Triphosphate↗

PubMed1991

Comparison of adenosine triphosphate- and nicotine-activated inward currents in rat phaeochromocytoma cells.

1. The adenosine triphosphate (ATP)-activated inward current was compared to the nicotine-activated inward current in nerve growth factor (NGF)-treated rat phaeochromocytoma PC12 cells. 2. Both ATP and nicotine activated an inward current at negative holding potentials. The concentration of ATP necessary to activate the inward current was about 10-fold higher than that of nicotine; the EC50 was 20.5 microM for ATP and 2.4 microM for nicotine. The maximal responses induced by ATP and nicotine were almost identical in the same cells. The current-voltage relationship for the ATP-activated current was very similar to that for the nicotine-activated current, and both currents reversed around 0 mV in a physiological saline. 3. The ATP-activated current and the nicotine-activated current were not additive; the current activated by a combined administration of ATP (100 microM) and nicotine (10 microM) was only about 20% larger than the current activated by either ATP or nicotine alone. Nicotine (100 microM) did not increase the current activated by 1 microM-ATP. 4. ATP could activate an inward current in the cells even after desensitization to nicotine had developed. 5. Hexamethonium (100 microM) selectively blocked the nicotine-activated current whereas suramin (100 microM), a purinoceptor antagonist, selectively blocked the ATP-activated current. 6. Ionic selectivity was studied by changing compositions of extracellular solutions. When external Na+ was replaced with Cs+, both ATP and nicotine activated inward currents. However, with an extracellular solution containing Tris or glucosamine as a major cation, only ATP, not nicotine, activated an inward current. 7. ATP- and nicotine-activated currents were also recorded from cells bathed in a solution containing 1.8 mM-Ca2+ as the only external cation, suggesting that both pathways are Ca2+ permeable. 8. The results suggest that the ATP-sensitive ionic pathway is not independent of the nicotine-sensitive pathway in these cells. Our working hypothesis is that ATP and nicotine activate the same channels but the binding sites and the open-states of the channels are different between these two agonists.

Adenosine Triphosphate↗

PubMed1987

Pre- and post-junctional effects of adenosine triphosphate on noradrenergic transmission in the rabbit ear artery.

1. The effects of adenosine triphosphate (ATP), 5'-adenylylimidodiphosphate (AMP-PNP) or alpha,beta-methylene ATP (mATP) on the excitatory junction potential (e.j.p.) and slow depolarization evoked by perivascular nerve stimulation were studied in smooth muscle cells of the rabbit ear artery. 2. ATP (above 10(-6) M), AMP-PNP (above 10(-6) M) and mATP (above 10(-8) M) transiently (10-15 min) depolarized the membrane. The membrane remained depolarized after prolonged exposure (over 20 min) to ATP (above 3 X 10(-5) M), AMP-PNP (above 10(-5) M) or mATP (above 3 X 10(-8) M). 3. ATP (above 10(-5) M), AMP-PNP (above 5 X 10(-6) M) or mATP (above 3 X 10(-8) M) decreased the membrane resistance. Increasing the external K+ concentration (K+o) to 10.1 mM also decreased the membrane resistance, with an associated depolarization. 4. ATP (10(-6)-5 X 10(-5) M) or AMP-PNP (over 10(-6) M) transiently decreased and then increased amplitudes of the e.j.p. and of the slow depolarization, the latter component increasing more than the former. 5. Depolarization of the membrane by 10.1 mM-K+o solution or mATP (10(-7) M) decreased the amplitude of e.j.p.s, with no change in the facilitation, and the slope of the relationship between amplitude of e.j.p. and that of slow depolarization decreased with mATP but not with 10.1 mM-K+o solution. 6. The outflows of noradrenaline and 3,4-dihydroxyphenylglycol (DOPEG) induced by perivascular nerve stimulation increased with ATP (above 10(-6) M) or AMP-PNP (above 10(-5) M), while there was no change with mATP (10(-8)-10(-5) M) or 10.1 mM-K+o solution. 7. Pre-treatment with mATP inhibited the ATP-induced increase in the outflow of noradrenaline and DOPEG, and also the ATP-induced enhancement of the amplitude of the e.j.p. 8. Therefore ATP and AMP-PNP have predominantly excitatory actions on both pre- and post-junctional membranes, while mATP has an excitatory action on the post-junctional membrane but antagonizes the facilitatory action of ATP on release of noradrenaline from the nerve terminal.

Action Potentials↗

PubMed2002

Potassium channels and human corporeal smooth muscle cell tone: diabetes and relaxation of human corpus cavernosum smooth muscle by adenosine triphosphate sensitive potassium channel openers.

PURPOSE: Sustained contraction of human corporeal smooth muscle depends on continuous transmembrane calcium flux through voltage gated calcium channels. K channels modulate corporeal smooth muscle membrane potential and, thus, ultimately affect transmembrane calcium flux. Therefore, we characterized relaxation responses elicited by the K channel modulators pinacidil and levcromakalim on isolated human corporeal tissue strips. We also evaluated the possibility that there may be alterations in adenosine triphosphate sensitive K channel pharmacology/function related to the presence of diabetes mellitus. MATERIALS AND METHODS: A total of 215 isolated human corporeal tissue strips obtained from 57 male patients with organic erectile dysfunction were investigated. Cumulative concentration-response curves were constructed at half log increments for steady state relaxation responses elicited by pinacidil and levcromakalim on equivalently phenylephrine pre-contracted (to approximately 75% of maximum) isolated corporeal tissue strips. Potassium currents were measured using the cell attached whole cell patch clamp technique on freshly isolated corporeal smooth muscle cells. RESULTS: A concentration dependent, glibenclamide sensitive relaxation response of phenylephrine pre-contracted corporeal tissue strips was observed for pinacidil and levcromakalim. Consistent with such observations, electrophysiological recordings on freshly isolated myocytes revealed that pinacidil (10 microM.) and levcromakalim (10 microM.) induced whole cell potassium currents that were blocked by glibenclamide (10 microM.). In addition, statistical analysis revealed that phenylephrine pre-contracted corporeal tissue strips from patients without diabetes were more sensitive to relaxation by both compounds than corporeal tissue strips excised from those with diabetes. Furthermore, relaxation responses elicited by pinacidil and levcromakalim were not affected by charybdotoxin or 4-aminopyridine but were completely reversed by KCl or tetraethylammonium chloride. CONCLUSIONS: These data indicate that the adenosine triphosphate sensitive K channel subtype is likely to have an important role in the relaxation of isolated corporeal tissue strips and, moreover, they are the molecular target for the K channel modulators/openers levcromakalim and pinacidil. Such observations are consistent with the supposition that alterations in the structure/function/activity of these potassium channels may underlie at least some aspects of observed diabetes related differences in tissue sensitivity to K channel modulators.

Adenosine Triphosphate↗

PubMed1995

Adenosine triphosphate and arachidonic acid stimulate glycogenolysis in primary cultures of mouse cerebral cortical astrocytes.

Adenosine triphosphate (ATP) promotes glycogenolysis in primary cultures of mouse cerebral cortical astrocytes with an EC50 of 1.5 microM. A pharmacological analysis indicates an involvement of purinergic P2Y receptors in this action of ATP. Application of either arachidonic acid (AA), or certain unsaturated fatty acids, also results in glycogen breakdown. The EC50 of AA is approximately 50 microM. Thus ATP and AA can be added to the list of neuroactive agents that control glycogen levels in astrocytes, which includes noradrenaline, vasoactive intestinal peptide (VIP), adenosine and histamine.

Adenosine Triphosphate↗

PubMed1975

Mood and whole blood adenosine triphosphate.

The claim of Hansen (1969) and Hansen and Dimitrakoudi (1974) that whole blood adenosine triphosphate (ATP) levels correlate with depressed affect was examined. The findings from 84 patients failed to confirm any relationship between mood and whole blood ATP. One patient showing the highest correlation (r = 0-85; p less than 0-001) between the ATP levels and mood in the original report was re-examined; no relationship was now found (r = -0-25; p greater than 0-1).

Adenosine Triphosphate↗

PubMed1976

Cyclization of the phosphorus chain of the methylene-bridged analogs of adenosine triphosphate.

The phosphorus-containing side chains of two methylene-bridged analogs of adenosine triphosphate have been cyclized to produce the corresponding analogs of monoadenosine-5'-trimetaphosphate. (The structures are given in the journal.) The molecules, which were generated in anhydrous media through a carbodimide-mediated condensation, were characterized by 31P nuclear-magnetic resonance, and the white-noise 1H decoupled spectra were simulated. These molecules are quite reactive and readily converted to their corresponding linear forms upon hydrolysis. The second structure contains an asymmetric phosphorus atom, and both of the possible cyclic molecules have been observed and the diasteroisomeric mixture has been isolated.

Adenosine Triphosphate↗

PubMed2004

Adenosine triphosphate stress myocardial contrast echocardiography detects coronary artery stenosis with greater sensitivity than wall-motion abnormality measurements.

BACKGROUND: Although stress myocardial contrast echocardiography (MCE) can be used to detect coronary stenosis, its efficacy relative to other methods, such as detection of wall-motion abnormalities, remains unknown. Thus, the goal of this study was to compare the sensitivity of MCE versus wall-motion abnormality detection in the assessment of coronary artery stenosis. METHOD: Nine dogs with severe but nonflow limiting stenosis in the circumflex coronary artery underwent evaluation with real-time MCE along the short-axis view during infusion of Optison. The equation of y = a (1 - e -betat ) + c, which fits the replenishment curve of MCE, was calculated in the midseptum (normal region) and in the lateral wall (ischemic region) before and during adenosine triphosphate infusion. Wall-motion abnormalities were also evaluated by visual assessment and by measurement of wall thickening. RESULTS: Area under the receiver operating characteristic curve in beta- and A x beta-value, and percent wall thickening, was 0.963, 0.963, and 0.889, respectively, indicating that the diagnostic accuracy for detecting the coronary artery stenosis by real-time MCE was higher than that by the wall-motion assessment. CONCLUSION: Real-time MCE has higher sensitivity in detecting coronary stenosis during adenosine triphosphate stress test when compared with wall-motion assessment.

Adenosine Triphosphate↗

PubMedDate not supplied

Platelet aggregation and adenosine triphosphate secretion in dogs with untreated multicentric lymphoma.

Whole-blood platelet aggregation and adenosine triphosphate secretion were measured in 15 dogs with untreated multicentric lymphoma and 10 normal control dogs to determine if dogs with lymphoma have altered platelet function. Dogs with quantitative platelet disorders (ie, thrombocytopenia or thrombocytosis) or with clinical evidence of a bleeding disorder were excluded from the study. Platelets from affected dogs had significantly greater maximum aggregation than those from control dogs, suggesting that platelets from dogs with lymphoma are hyperactive. Platelet hyperactivity may play a role in the development of hemostatic disorders (eg, disseminated intravascular coagulation) or in tumor metastasis. Further investigation is needed to determine if modification of platelet function in patients with lymphoma affects disease progression or outcome.

Adenosine Triphosphate↗

PubMed1987

Effect of X irradiation on adenosine triphosphate and glucose-6-phosphate dehydrogenase in the CaNT mouse tumor.

The levels of adenosine triphosphate (ATP) in the transplantable CaNT murine tumor grown in CBA mice at various times following 5, 10, and 15 Gy X rays (100 kVp) were increased within 45 min. Maximal ATP levels occurred at 2.5 h following the 10 Gy dose (3.8 times that of unirradiated controls), returning almost to control levels by 13 h after irradiation. The specific activity of glucose-6-phosphate dehydrogenase (G-6-PDH) after 10 Gy increased about 1.5-fold 1 h after irradiation, returning to control levels by 48 h. It is suggested that the increased ATP following irradiation might play a major role in energy provision when cellular repair processes are able to operate. The increased G-6-PDH activity after irradiation may reflect enhanced metabolism associated with cellular repair mechanisms.

Adenosine Triphosphate↗

PubMed2001

Regeneration of adenosine triphosphate from glycolytic intermediates for cell-free protein synthesis.

A new approach for adenosine triphosphate (ATP) regeneration in a cell-free protein synthesis system is described. We first show that pyruvate can be used as a secondary energy source to replace or supplement the conventional secondary energy source, phosphoenol pyruvate (PEP). We also report that glucose-6-phosphate, an earlier intermediate of the glycolytic pathway, can be used for ATP regeneration. These new methods provide more stable maintenance of ATP concentration during protein synthesis. Because pyruvate and glucose-6-phosphate are the first and last intermediates of the glycolytic pathway, respectively, the results also suggest the possibility of using any glycolytic intermediate, or even glucose, for ATP regeneration in a cell-free protein synthesis system. As a result, the methods described provide cell-free protein synthesis with greater flexibility and cost efficiency.

Adenosine Triphosphate↗