INFRARED SPECTRA OF ADENOSINE TRIPHOSPHATE COMPLEXES IN AQUEOUS SOLUTION.
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Adenosine Triphosphate↗
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Response of the intracellular adenosine triphosphate pool of Saccharomyces cerevisiae to growth inhibition induced by excess L-methionine.
Yeast cells accumulate S-adenosyl-l-methionine (S-AM) when cultivated in the presence of l-methionine. Cell growth is inhibited by the addition of high concentrations of l-methionine. A number of investigators have attributed this to the depletion of adenosine triphosphate (ATP) as a consequence of the utilization of that mucleotide for S-AM formation. The cellular ATP pool of Saccharomyces cerevisiae was measured during growth inhibition caused by addition of excess l-methionine. Polyethylenimine thin-layer chromatography and subsequent autoradiography were used to quantitate the extracted ATP. Addition of l-methionine to a level of 5 mg/ml in a culture during exponential growth caused an increase in the doubling time of 40 to 50%. During this period, the cellular ATP level continued increasing normally and, as the cells entered stationary growth, receded to a level characteristic of an uninhibited stationary culture growth. After the addition of methionine, there was never an observed depletion of the ATP pool other than the normal fluctuation which occurs in an uninhibited culture. We have concluded that growth inhibition by excessive methionine does not result from limiting availability of ATP.
Adenosine Triphosphate↗
Adenosine triphosphate and phosphocreatine levels in cochlear structures. Use rate and effect of salicylates.
Guinea pigs were injected with various dosages of salicylate for varying time periods. The temporal bones were removed, frozen quickly, freeze-dried, and the cochlea was dissected into essential auditory component parts and subjected to microchemical analysis for phospho-creatine (P-creatine) and adenosine triphosphate (ATP) levels. It was found that high energy phosphates were not decreased by therapeutic or acutely toxic levels of salicylate. Only when chronic intoxication with salicylate was accomplished was there a reduction in ATP and P-creatine. The data presented do not provide support for the widely held view that uncoupling of oxidative phosphorylation or inhibition of enzymes involved in energy generation in the inner ear structures studied (organ of Corti, stria vascularis, Reissner's membrane, modiolar blood vessels, cochlear nerve and spiral ganglion) are the mechanisms by which salicylates cause reversible hearing loss. The study confirms the existence of a P-creatine gradient opposite to the well known glycogen gradient in the organ of Corti (Krzanowski JJ Jr, Matschinsky M: J Histochem 19:321, 1971) and suggests a relatively uniform energy use rate of this tissue for all four turns (20 mmoles of approximately phosphorus used/kg dry weight/min).
Adenosine Triphosphate↗
THE NON-ENZYMATIC TRANSPHOSPHORYLATION OF LOWER ALIPHATIC ALCOHOLS BY ADENOSINE TRIPHOSPHATE.
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Adenosine Triphosphate↗
Computer-assisted analysis of adenosine triphosphate data.
A computer program has been written to assist in the analysis of adenosine 5'-triphosphate data. The program is designed to calculate a dilution curve and to correct sample and adenosine 5'-triphosphate standard data for background and dilution effects. In addition, basic statistical parameters and estimates of biomass carbon are also calculated for each group of samples and printed in a convenient format. The versatility of the program to analyze data from both qauatic and terrestrial samples is noted as well as its potential use with various types of instrumentation and extraction techniques.
Adenosine Triphosphate↗
Effect of prostacyclin and adenosine triphosphate on vasospasm of canine basilar artery.
Cerebral vasospasm is one of the most important factors influencing morbidity and mortality of intracranial operations or diseases. Platelet aggregation and adhesion is increased in spastic vessels. Degradation of platelets liberates mediators, which in turn increase vasospasm, thus creating a vicious cycle. Healthy vessels cope with this by increasing the synthesis of prostacyclin. The purpose of this study was to increase experimentally the levels of arterial prostacyclin and adenosine triphosphate (ATP) in animals through intraarterial injection of these substances because they are lower in spastic vessels. Prostacyclin promotes antiaggregation and dilatation, increases blood flow, inhibits thromboxane A2, and prevents synthesis of angiotensin II. Most of these effects were done by increasing cyclic adenosine monophosphate (cAMP). After injecting autogenous blood into the cisterna magna of male dogs, both the acute and chronic phases of vasospasm and the degenerative changes in the arterial wall were observed. Injecting ATP increased the severity of vasospasm. During vasospasm it was found that when prostacyclin is used intraarterially, vasodilatation began, but degeneration of the arterial wall could not be prevented. In the group of animals in which both ATP and prostacyclin were used, there was no degeneration of the arterial wall and the basilar artery was seen to be normal when viewed under the electron microscope.
Adenosine Triphosphate↗
Improved tolerance to ischemia in hypertrophied myocardium by preischemic enhancement of adenosine triphosphate.
In prior studies from this laboratory to determine the mechanisms whereby hypertrophied myocardium is more sensitive to ischemic injury than normal myocardium, it was demonstrated that hypertrophied rat hearts have lower basal high-energy phosphate levels and develop ischemic contracture sooner than normal myocardium. The purposes of this study were (1) to determine if the decrease in myocardial adenosine triphosphate (ATP) was associated with the increased rate of ischemic contracture and (2) to determine if arrest and perfusion of hypertrophied myocardium prior to the ischemic interval would allow recovery of high-energy phosphate stores and improve tolerance to ischemia. ATP levels were measured in isolated normal and hypertrophied rat hearts during (1) control nonworking Langendorff perfusion, (2)2 minutes of potassium chloride-arrested perfusion (30 mEq/L), or (3) 15 minutes of potassium chloride-arrested perfusion (30 mEq/L). Both groups were then made globally ischemic (37 degrees C) and the time to ischemic contracture recorded. Hypertrophied hearts were produced by permanent banding of the ascending aorta and confirmed by left ventricular (mg) body weight (gm) ratios (normal, 1.95 wet, p less than 0.05). After 2 minutes of mechanical arrest the time to ischemic contracture was increased 75% +/- 10% in normal and 44% +/- 4% in hypertrophied hearts. After 15 minutes of mechanical arrest with perfusion, hypertrophied myocardium re-established normal ATP levels and increased its time to ischemic contracture by 130% +/- 7%. These studies suggest that during potassium chloride arrest, additional preischemic metabolic recovery is possible by hypertrophied myocardium and leads to increased tolerance to ischemia beyond that accomplished by cessation of mechanical activity alone. This effect is seen only to a minor degree in normal myocardium.
Adenosine Triphosphate↗
Phosphoarginine-adenosine triphosphate exchange detected in vivo in a microscopic nematode parasite by flow 31P FT-NMR spectroscopy.
In vivo flow 31P NMR spectroscopy of a microscopic nematode, Steinernema carpocapsae, is described. Long-term viability was maintained during analysis by continuous circulation of an oxygenated suspension of the parasite through an NMR spectrometer. Saturation transfer and inversion recovery were employed under flowing conditions to investigate the kinetics of phosphoarginine<-->adenosine triphosphate exchange. The kinetic constants for the forward and reverse reactions were 0.37/s and 1.45/s, respectively. This report is the first to demonstrate a functional phosphagen kinase in the metabolism of a parasitic helminth.
Adenosine Triphosphate↗
Further observations on the utilization of adenosine triphosphate in rat mast cells during histamine release induced by the ionophore A23187.
1 The relation between A23187-induced histamine release and the energy metabolism of the rat mast cells has been studied. 2 Ethacrynic acid was used as an inhibitor of calcium-induced histamine release from mast cells primed with the ionophore A23187, and to study calcium-induced changes in the adenosine triphosphate (ATP) content and the rate of lactate production of A23187-primed mast cells. 3 Ethacrynic acid by itself decreased the rate of glycolytic ATP production. 4 By measurement of the ATP content and the lactate production of mast cells with or without secretory activity, the increased demand of energy for exocytosis was estimated to be equivalent to 0.14 pmol of ATP pr 10(3) mast cells.
Adenosine Triphosphate↗
Analysis of the contractile responses of the ileal segment of the isolated blood-perfused small intestine of rats to adenosine triphosphate and related compounds.
For close-arterial injection the isolated small intestine of the rat was perfused by a cross-circulation technique at a fixed flow rate through the superior mesenteric artery with arterial blood from a donor. Single intra-arterial injections of purine derivatives elicited a monophasic fast contraction of the ileum. In order to elucidate the mechanism of the fast contraction, adenosine triphosphate (ATP) was chosen for further investigations. The ileal response to ATP was abolished by tetrodotoxin, hexamethonium or morphine, but was resistant to blockade by atropine, methysergide or mepyramine. These results definitely indicate that ATP causes the fast contraction of the ileum by a stimulation of neuronal elements in the myenteric plexus involving cholinergic interneurons.
Adenine Nucleotides↗
[Adenosine triphosphate for supraventricular tachycardia in newborns and suckling infants].
A previously healthy and normally developing 12-day-old female suddenly became restless and developed cold sweats, tachypnoea and tachycardia (300 beats/min). Neither electrocardiogram nor echocardiogram showed evidence of any cardiac defect. Carotid sinus massage and other vagus-stimulating manoeuvres, undertaken because paroxysmal supraventricular tachycardia (PSVT) was suspected, were unsuccessful. Before rapid digitalization, adenosine triphosphate was administered (0.1 mg/kg intravenously). Sinus rhythm was restored within about 60 s. Despite further treatment with digoxin and verapamil (4 mg/kg.d), further episodes of PSVT occurred, each again responding to ATP (0.1 to 0.3 mg/kg). There were no side effects. After 24-hour Holter ECG monitoring had revealed Wolff-Parkinson-White syndrome as cause of the PSVT, propafenone was administered (15 mg/kg daily) and has prevented further recurrence of the tachycardia.
Adenosine Triphosphate↗
The effects of adenosine triphosphate (ATP) and related purines on human isolated subcutaneous and omental resistance arteries.
1. Human resistance arteries were obtained from specimens of omentum and subcutaneous fat removed at surgery. They were studied in vitro by use of a myograph technique to determine the effects of purines on the arteries. 2. In preparations where tone had been raised with noradrenaline, low concentrations (1 nM-1 microM) of adenosine triphosphate (ATP) and 2-methylthioATP, but not alpha,beta-methyleneATP, produced concentration-dependent relaxation. There was a lack of relationship between the relaxation response to acetylcholine and that to ATP. 3. In preparations under basal tone, high concentrations (1 microM-1 mM) of ATP, 2-methylthioATP and alpha,beta-methyleneATP produced concentration-dependent contractions. 4. The rank order of potency of the purine nucleotide analogues for the relaxation response was 2-methylthioATP > ATP > alpha,beta-methyleneATP and for the contractile response it was alpha,beta-methyleneATP > ATP = 2-methylthioATP. 5. Adenosine produced concentration-dependent relaxation in preparations under raised tone and was less potent than ATP but did not produce contraction in preparations at basal tone. Relaxation responses to adenosine, but not to ATP, were antagonized by 8-phenyltheophylline. 6. These results indicate the presence of vasodilator P2y- and P1-purinoceptors and vasoconstrictor P2x-purinoceptors on human resistance arteries isolated from omental and subcutaneous sites.
Adenosine Triphosphate↗
Dissimilarity between the responses to adenosine triphosphate or its related compounds and non-adrenergic inhibitory nerve stimulation in the longitudinal smooth muscle of pig stomach.
1 Transmural electrical stimulation (TMS) of longitudinal smooth muscle strips taken from the cardiac portion of the pig stomach produced biphasic responses consisting of initial contractions followed by relaxations. The excitatory component was enhanced by neostigmine and abolished by atropine. After atropine treatment, TMS and nicotine or 1,1-dimethyl-4-phenyl-piperazinium, caused a relaxation or a relaxation followed by an after-contraction. All of these responses were abolished or reduced reversibly with tetrodotoxin and cocaine, while hexamethonium only abolished the response to ganglion-stimulating agents.2 The relaxation caused by TMS reached a maximum amplitude at 5-10 Hz, and was entirely resistant to the effects of alpha- and beta-adrenoceptor blocking agents, or a combination of them, and also to guanethidine. These results strongly suggested that the relaxation was elicited by stimulation of intramural non-adrenergic inhibitory neurones.3 In the presence of atropine and guanethidine, adenosine triphosphate (ATP, 5-20 muM) caused only a tonic contraction, and ATP (25-200 muM) or adenosine diphosphate (25-200 muM) produced a contractile response or a biphasic one (tonic contraction preceded by a slight relaxation). Adenosine monophosphate and adenosine caused only the tonic contraction over the range of concentrations (25-200 muM).4 Stimulation of the intramural inhibitory neurones of the tissue consistently evoked an inhibitory junction potential, which showed a summation during repetitive stimulation. One the other hand, ATP elicited mainly a small depolarization of a few mV.5 When the desensitization to ATP of the muscle was achieved in the presence of atropine and guanethidine, the relaxation induced by stimulation of the non-adrenergic inhibitory neurones could be evoked without any modification.6 Dipyridamole neither potentiated the inhibitory responses due to stimulation of the intramural inhibitory neurones nor showed any consistent effect on the ATP-induced response.7 From these results, it is unlikely that ATP, or any related compound, is the transmitter substance of the intramural inhibitory neurones in the longitudinal smooth muscle of the pig stomach.
Adenosine Triphosphate↗
Effects of adenine nucleotides and phosphate on adenosine triphosphate sulphurylase from Anabaena cylindrica.
Production of adenosine 5'-[35S]sulphatophosphate by a partially purified ATP sulphurylase from Anabaena cylindrica was inhibited by AMP, ADP and P1. Decreases in enzyme activity in the presence of these inhibitors were reversed by increasing the concentrations of ATP. The adenine nucleotides inhibited the enzyme competitively with respect to ATP. In the presence of P1, ATP showed a positive co-operative effect on enzyme activity. The inhibition by P1 was enhanced by increasing concentrations of MG2+. The effects of the adenine nucleotides and the interaction of P1 and Mg2+ on ATP sulphurylase activity are discussed in relation to the regulation of sulphate assimilation via the energy metabolism of the alga.
Adenine Nucleotides↗
Role of exogenous adenosine triphosphate in catabolic and synthetic activities of Chlamydia psittaci.
The synthetic activities of isolated cells of the meningopneumonitis strain (MN) of Chlamydia psittaci were investigated and further observations were made on their catabolic reactions. These observations included the demonstration of CO(2) production from aspartate in the presence of pyruvate and the formation of pyruvate from glucose-6-phosphate. Both reactions were enhanced by added adenosine triphosphate (ATP). Of a large number of compounds tested, only glucose-6-phosphate, pyruvate, aspartate, and isoleucine were shown to furnish carbons that were incorporated into molecules precipitated by trichloroacetic acid. The reactions with pyruvate, aspartate, and isoleucine were dependent entirely, or almost entirely, on added ATP, and the reaction with glucose-6-phosphate was enhanced by ATP. Except for CO(2), which greatly stimulated the reactions, the addition of a number of other compounds or a combination of compounds, such as cofactors, amino acids, and purine and pyrimidine bases, did not greatly affect incorporation. About 95% of the activity of the trichloroacetic acid precipitates was recovered in the chloroform-methanol soluble fraction.
Acetates↗
Impairment of endothelium-dependent vasodilation induced by acetylcholine and adenosine triphosphate following experimental subarachnoid hemorrhage.
The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of isolated rabbit basilar artery was examined using an isometric tension recording method. Thirty-five rabbits that had 2 successive blood injections were divided into 3 groups: normal animals (control), 4 days, and 3 weeks after the first SAH. Acetylcholine (ACh) (10(-6)-10(-4) M) and adenosine triphosphate (ATP) (10(-6)-10(-4) M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10(-6) M serotonin. In the animals killed 4 days after the first SAH, both ACh- and ATP-induced relaxation were suppressed, and the degree of relaxation of this group was 38 +/- 4.5% (mean +/- SEM) and 22 +/- 3.9% of the initial contractile tone in response to 10(-4) M ACh and 10(-4) M ATP, respectively. Suppression of the relaxation induced by ATP was seen even in the animals killed 3 weeks after the first SAH. Moreover, pretreatment with hemoglobin (10(-6) and 10(-5) M) inhibited endothelium-dependent vasodilation induced by ACh in the arterial rings from the animals killed 4 days after the first SAH. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH may be involved in the pathogenesis of cerebral vasospasm.
Acetylcholine↗
Assessing the risk of infection and rejection in Hispanic renal transplant recipients by means of an adenosine triphosphate release assay.
INTRODUCTION: Because of the necessary immunosuppression, transplant recipients have a high risk of infection. Conversely, underimmunosuppression carries with it the risk of rejection. It would be quite useful to have a test that could differentiate between infection and rejection in renal transplant patients and better still, to predict which patients are at risk of complications. A new assay, which measures adenosine triphosphate (ATP) synthesis by CD4+ T cells in response to stimulation by phytohemagglutinine (Immuknow assay, Cylex, Inc) is undergoing clinical evaluations. Preliminary investigations suggest that this test could be useful to assess and predict the immune status of patients with other conditions. METHODS: We examined the records of all patients who received a kidney transplant in our program between August 2004 and January 2005. Of 64 patients, 58 had pretransplant and posttransplant ATP level determinations. We searched for associations between ATP levels and immunosuppression type, doses, and levels; creatinine levels; white blood cell count; tissue typing; preformed antibodies; as well as ATP levels on infection and rejection, and changes in ATP levels with time. Chi-square, Fisher, t test, analysis of variance (ANOVA), and relative risks were used for analysis of data. RESULTS: There was no relation between ATP levels and immunosuppression type, doses, or levels; creatinine levels; white blood cell counts; HLA; and panel-reactive antibody (P > 0.05). However, patients with moderate or high pretransplant ATP levels had more rejection episodes (8/10) while patients with ATP levels in the low immune response had more infections (6/11) (P < .001; relative risk [RR] for rejection = 1.2; RR for infection = 4.4). The mean ATP levels for rejection was 423.3 ng/mL versus 268.45 ng/mL for infection and 277.15 ng/mL for no events (ANOVA, P = .0145). Although acute rejections occurred mostly above 300, this was not significant (P = .059; RR = 0.9). Infections were more frequent with ATP under 300 (RR = 7.3) and severe infection (endocarditis, meningitis, peritoneal abscesses, pneumonia, etc) were more frequent under 200 (P < .001). Comparing pretransplant with posttransplant values at the second week an increase correlated with rejection (P < .001, RR = 15.3), while a decrease did not correlate with the infection (P = .845, RR = 1.4). Patients who received antirejection treatment had a decrease in their ATP levels at 5 days (P = .002). CONCLUSION: This ATP release assays helpful in determining the risk of developing infection or rejection, as well as follow-up in the response to therapy.
Adenosine Triphosphate↗
Effects of muscular exercise on erythrocyte adenosine triphosphate concentration in patients with insulin-dependent diabetes mellitus.
Type I diabetes mellitus represents a metabolic disorder in which intracellular glycolytic pathway is inhibited by insulin deficiency, with the subsequent decreased availability of energetic substrates such as ATP. Some aspects of the energetic metabolism in response to an intensive demand (muscular exercise) were investigated, in a group of 10 ketotic diabetic patients, by measuring erythrocyte adenosine triphosphate (ATP) and blood glucose, free fatty acids (FFA) and lactate levels. In the diabetic subjects, in comparison with normal subjects, the decreased levels of erythrocyte ATP at rest did not increase after exercise, while the increased levels of FFA at rest did not diminish after exercise. The results show that the impaired erythrocyte glycolysis may produce reduced levels of ATP not only at rest, but also after exercise, when muscular contraction results in a manifold increase in cellular energy requirements. In addition, other metabolic systems providing energy for the exercising muscle, such as FFA utilization, are impaired in the ketotic diabetic patients.
Adenosine Triphosphate↗