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PubMed1990

Relationships between the neuronal sodium/potassium pump and energy metabolism. Effects of K+, Na+, and adenosine triphosphate in isolated brain synaptosomes.

The relationships between Na/K pump activity and adenosine triphosphate (ATP) production were determined in isolated rat brain synaptosomes. The activity of the enzyme was modulated by altering [K+]e, [Na+]i, and [ATP]i while synaptosomal oxygen uptake and lactate production were measured simultaneously. KCl increased respiration and glycolysis with an apparent Km of about 1 mM which suggests that, at the [K+]e normally present in brain, 3.3-4 mM, the pump is near saturation with this cation. Depolarization with 6-40 mM KCl had negligible effect on ouabain-sensitive O2 uptake indicating that at the voltages involved the activity of the Na/K ATPase is largely independent of membrane potential. Increases in [Na+]i by addition of veratridine markedly enhanced glycoside-inhibitable respiration and lactate production. Calculations of the rates of ATP synthesis necessary to support the operation of the pump showed that greater than 90% of the energy was derived from oxidative phosphorylation. Consistent with this: (a) the ouabain-sensitive Rb/O2 ratio was close to 12 (i.e., Rb/ATP ratio of 2); (b) inhibition of mitochondrial ATP synthesis by Amytal resulted in a decrease in the glycoside-dependent rate of 86Rb uptake. Analyses of the mechanisms responsible for activation of the energy-producing pathways during enhanced Na and K movements indicate that glycolysis is predominantly stimulated by increase in activity of phosphofructokinase mediated via a rise in the concentrations of adenosine monophosphate [AMP] and inorganic phosphate [Pi] and a fall in the concentration of phosphocreatine [PCr]; the main moving force for the elevation in mitochondrial ATP generation is the decline in [ATP]/[ADP] [Pi] (or equivalent) and consequent readjustments in the ratio of the intramitochondrial pyridine nucleotides [( NAD]m/[NADH]m). Direct stimulation of pyruvate dehydrogenase by calcium appears to be of secondary importance. It is concluded that synaptosomal Na/K pump is fueled primarily by oxidative phosphorylation and that a fall in [ATP]/[ADP][Pi] is the chief factor responsible for increased energy production.

Adenosine Triphosphate↗
PubMed1993

[The diagnostic and therapeutic utility of adenosine triphosphate in supraventricular tachyarrhythmias in childhood].

The diagnostic and therapeutic utility of adenosine triphosphate (ATP) in pediatric age was investigated in fifteen children aged 4 days-16 years (mean age 6.4 years) observed for paroxysmal (Group A-9 pts) or incessant (Group B-6 pts) tachycardia. Twelve patients underwent transesophageal electrophysiological study. ATP was given as an intravenous bolus (0.075-0.5 mg/Kg). In Group A patients, ATP resulted in termination of spontaneous or induced tachycardia, and in all cases interruption in anterograde limb of the re-entry circuit occurred. In Group B patients, ATP induced transient atrioventricular block with persistence of atrial tachycardia, suggesting the atrial origin of the arrhythmia. No adverse haemodynamic effects were observed in any patient. We conclude that in pediatric age ATP must be considered the drug of first choice for junctional reciprocating tachycardias because of its efficacy, short mid-life and insignificant side-effects. Furthermore, it represents an effective diagnostic test for differentiating between junctional reciprocating tachycardias and atrial ectopic tachycardias.

Adenosine Triphosphate↗
PubMed1998

Effect of adenosine triphosphate on human coronary circulation.

We investigated in humans the effects of adenosine triphosphate (ATP), administered by intracoronary bolus (4-16 microg) or intravenous infusion (25-200 microg/kg/min), on coronary and systemic hemodynamics and electrocardiogram (ECG) variables. All patients had normal epicardial coronary arteries. The maximal coronary blood flow velocity (CBFV) was determined with intracoronary bolus of papaverine. A 12 microg bolus of ATP (n=12) caused maximal coronary hyperemia similar to that caused by papaverine. Intracoronary boluses caused a small brief decrease in arterial pressure but no significant changes in HR or ECG variables. Intravenous infusion of ATP at 150 microg/kg/min (n=15) caused a decrease in the coronary resistance index similar to that caused by papaverine, but the rate of increase in CBFV by ATP was smaller than that caused by papaverine. No patients had a significant change in ECG variables, but some patients (40%) had a serious decrease in arterial pressure. These studies suggest that maximal coronary vasodilation can be achieved safely with intracoronary ATP administration and that intravenous infusions at 150 microg/kg/min cause near-maximal coronary hyperemia in most patients.

Adenosine Triphosphate↗
PubMed1965

Adenosine Triphosphate and Other Requirements for the Utilization of Glucose by Agents of the Psittacosis-Trachoma Group.

Weiss, Emilio (Naval Medical Research Institute, Bethesda, Md.). Adenosine triphosphate and other requirements for the utilization of glucose by agents of the psittacosis-trachoma group. J. Bacteriol. 90:243-253. 1965.-The agent of meningopneumonitis cultivated in the allantoic cavity of chick embryos and purified by differential centrifugations was employed for most of the studies of the requirements for glucose utilization. The evolution of C(14)O(2) from glucose-1-C(14) was used as the criterion of metabolic activity in most experiments. The rate of glucose utilization increased somewhat during the first hour of incubation at 34.4 C and became approximately constant during the second hour. Changes in glucose concentration from 1 to 5 mm did not appreciably affect metabolic activity. More vigorous CO(2) production was obtained when the ratio of K(+)-Na(+) was >1 and, under certain conditions, when the concentration of inorganic phosphate was relatively high (0.05 m). Glucose utilization was entirely dependent on added adenosine triphosphate (ATP) and Mg(++). The effect of ATP was greatly reduced when the microorganisms were partially disrupted with sonic energy. Adenosine diphosphate (ADP) could be substituted for ATP, but the activity was reduced to less than 20%. ATP was not required when glucose-6-phosphate was substituted for glucose. With ADP and glucose, glucose-6-phosphate was an effective competitor of glucose utilization. Nicotinamide adenine dinucleotide phosphate (NADP) enhanced CO(2) production from carbon 1, but not from other carbons, with glucose and, especially, glucose-6-phosphate as substrates. ATP and NADP produced the above-described effects only when their concentrations were comparable to those of the substrates. These concentrations always exceeded the amount of CO(2) produced (0.05 to 0.5 mumole/mg of agent protein). The concentration of NADP could be reduced when oxidized glutathione was added. Diphosphothiamine had no effect on CO(2) production. Qualitatively similar results were obtained with the agent of trachoma purified from yolk sac. These experiments furnish evidence that agents of the psittacosistrachoma group, despite their enzymatic capabilities, require an exogenous source of energy.

Journal Article↗
PubMed1989

Adenosine triphosphate blocks opiate withdrawal symptoms in rats and mice.

The effect of adenosine triphosphate (ATP) on the expression of opiate withdrawal was examined using a chronic model of morphine-dependence. ATP was studied for its ability to modify or block jumping in morphine-abstinent mice. In mice administered 2 mg/kg ATP intravenously, the naloxone ED50 for withdrawal jumping increased by 11-fold in comparison to saline-treated mice. Nalaxone-precipitated morphine-withdrawal in the rats, has been shown to induce a specific pattern of intestinal hypermyoelectric activity and to increase the arterial blood pressure. Administration of ATP at dose of 1 and 2 mg/kg intravenously inhibited the induction of hypermyoelectric activity pattern in 80 and 100% of animals tested respectively. ATP also blocked the increase in mean arterial blood pressure seen during withdrawal in a dose-dependent fashion. Investigations were carried out to determine if blocking of the alpha 2-adrenoreceptors with yohimbine would result in an alteration in antiwithdrawal action of ATP. Yohimbine reversed the effect of ATP in blocking naloxone-precipitated withdrawal on the myoelectric activity of jejunum and colon, however, it failed to antagonize the effect of ATP on withdrawal jumping and to block the effect of ATP on the pressor response produced by naloxone in morphine-dependent animals.

Adenosine Triphosphate↗
PubMed1989

Kinetics of contraction initiated by flash photolysis of caged adenosine triphosphate in tonic and phasic smooth muscles.

Laser flash photolysis of caged adenosine triphosphate (ATP), in the presence of Ca2+, was used to examine the time course of isometric force development from rigor states in glycerinated tonic (rabbit trachealis) and phasic (guinea-pig ileum and portal vein) smooth muscles. Photolytic liberation of ATP from caged ATP initiated force development, at 20 degrees C, with half-time (t1/2) of 5.4 s in trachealis and 1.2-2.2 s in the phasic muscles. Prior to photolysis, some muscles were phosphorylated with ATP plus okadaic acid (an inhibitor of myosin light-chain phosphatase) or thiophosphorylated with ATP gamma S to fully activate the regulatory system, before turning on the contractile apparatus. In these prephosphorylated muscles, force development, after caged ATP photolysis, was more rapid than in the unphosphorylated muscles, but the t1/2 values for trachealis (0.8-1.1 s) were still longer than for ileum and portal-vein muscles (0.20-0.25 s). The results suggest that both the contractile machinery and the regulatory system are slower in the tonic than in the phasic smooth muscles. The time course of force development for each muscle type was sigmoidal, with an initial delay (td) of approximately 10% of the t1/2 value. Some possible chemical and mechanical origins of the delay are discussed.

Adenosine Triphosphate↗
PubMed1987

Action of externally applied adenosine triphosphate on single smooth muscle cells dispersed from rabbit ear artery.

1. Adenosine triphosphate (ATP), applied in the bathing solution or ionophoretically, depolarized freshly dispersed single arterial smooth muscle cells obtained by collagenase and elastase treatment of the rabbit ear artery. 2. Ionophoretic application of ATP evoked an inward current with a latency of about 70 ms and a time to peak of about 230 ms in cells held under voltage clamp using whole-cell patch-pipette techniques. 3. Bath application of 10 microM-ATP evoked a transient inward current at negative holding potentials. The amplitude of the ATP-induced current was linearly related to the clamp potential with a reversal potential near 0 mV. Removal of extracellular calcium, buffering intracellular calcium with high EGTA concentration, or depleting calcium stores with caffeine or noradrenaline treatment did not affect the ATP-evoked current. 4. Changing the chloride concentration gradient by decreasing extracellular or intracellular chloride concentration, or using the chloride channel blocker, frusemide, had no effect on the currents. 5. Replacing sodium with Tris shifted the reversal potential to more negative potentials. The reversal potential was not affected by exchanging intracellular potassium for caesium or sodium. Replacing extracellular sodium with 89 mM-barium also had little effect on the reversal potential. 6. These results are consistent with ATP activating a conductance that is cation selective but allows both monovalent and divalent cations to pass across the membrane.

Action Potentials↗
PubMed2006

Adenosine triphosphate inhibits endothelin-1 production by rat inner medullary collecting duct cells.

Adenosine triphosphate (ATP) and endothelin (ET)-1 inhibit vasopressin-stimulated water reabsorption in the inner medullary collecting duct (IMCD). Because both ATP and ET-1 are released by the IMCD and can act in an autocrine manner to regulate IMCD water transport, we sought to determine whether these factors can modulate the other's production. To begin such studies, the effect of ATP on IMCD ET-1 production was examined. ATP caused a dose-dependent inhibition of ET-1 release and inhibited ET-1 mRNA levels in primary cultures of rat IMCD cells. This effect was first evident after 4 hrs of exposure to ATP and persisted for at least 24 hrs. The 50% inhibitory concentration for ATP inhibition of ET-1 production was approximately 1 microM, and the maximal response was observed at 25-100 microM. ATP acted, at least in part, through the P2Y2 receptor because its effect was mimicked by UTP, but not by the P2X agonist, alpha,beta-methylene-ATP. N-methyl-L-arginine, or indomethacin, did not block the ATP inhibitory effect. In summary, these data demonstrate that ATP inhibits IMCD ET-1 protein and mRNA accumulation, that this is mediated via P2Y receptors, and that the ATP effect is independent of cyclooxygenase or nitric oxide synthase metabolites. These findings suggest that although ATP and ET-1 both antagonize vasopressin action in the IMCD, they may have a complex interaction that ultimately determines the degree to which they each participate in modulating collecting duct function.

Adenosine Triphosphate↗
PubMed2000

Biliary indocyanine green excretion as a predictor of hepatic adenosine triphosphate levels in patients with obstructive jaundice.

BACKGROUND: Correlation of the hepatic adenosine triphosphate (ATP) level with indocyanine green (ICG) excretion into bile was examined in patients with obstructive jaundice after the relief of hyperbilirubinemia by preoperative percutaneous transhepatic biliary drainage (PTBD). METHODS: Patients with complete bile duct obstruction, the mean serum total bilirubin concentration being 13.6 +/- 8.5 (SD) mg/dL, underwent PTBD prior to surgery. Within a few days before surgery when the mean serum total bilirubin level decreased to 1.2 mg/dL, ICG (0.5 mg/kg) was intravenously injected, and the whole bile was collected at 1-hour intervals for 5 hours. The ICG concentration in bile, bile flow rate, amount of ICG excreted in bile, and biliary ICG excretion rate as percentage of the injected dose were determined. At the time of surgery, a small liver tissue sample was obtained immediately after laparotomy without any ischemic procedures, and ATP concentrations were determined. Results of hepatic ATP levels were correlated with laboratory and clinical determinations. RESULTS: The bile flow rate was essentially constant during the 5-hour period, the mean value being 21 mL/hour. The ICG concentrations in bile gradually increased, reached the maximal level in 3 hour, and declined thereafter. The biliary ICG excretion rate for 5 hours was 40% +/- 18% of its injected dose. The biliary ICG excretion rate and amount of ICG excreted in bile for 5 hours significantly (P <0.05) correlated with the hepatic ATP level. The decline index of serum bilirubin during PTBD was also correlated with the hepatic ATP level. The serum ICG retention rate, bile flow rate, maximal ICG concentration in bile, and other liver function tests including serum albumin and cholinesterase levels did not correlate with the hepatic ATP level. CONCLUSIONS: Both the amount of and excretion rate of ICG in bile reflect the hepatic ATP level. Determination of biliary ICG excretion contributes to precise evaluation of hepatic energy status before surgery in patients with obstructive jaundice.

Adenosine Triphosphate↗
PubMed1995

Alteration of adenosine triphosphate and other nucleotides after sublethal oxidant injury to rat type II alveolar epithelial cells.

The alveolar epithelial cells of the lower respiratory tract are continuously exposed to injurious agents, including oxygen radicals. The type II alveolar epithelial cell is critically important to the normal function of the lung, because it is responsible for synthesis of surfactant and other essential duties. The present investigation measured the level of intracellular nucleotides and adenosine over time after exposure of type II cells to sublethal concentrations of physiologically relevant oxidants, hydrogen peroxide and hypochlorous acid (HOCl). Initially, it was determined that 250 microM HOCl or 250 microM hydrogen peroxide could each cause sublethal injury to the type II cells after exposure of up to 1 and 2 hours, respectively. After exposure to 250 microM hydrogen peroxide, the intracellular levels of adenosine, adenosine diphosphate, and adenosine triphosphate all initially increased in the first 1 to 15 minutes, but subsequently decreased significantly, ultimately reaching close to 40% below control levels. The level of adenosine monophosphate remained significantly elevated throughout the exposure until returning to control levels after 2 hours. Similar results occurred after the type II cells were exposed to 250 microM HOCl. This study demonstrates that adenosine triphosphate and other cellular nucleotides and nucleosides were decreased in type II cells before lethal injury and subsequent cell death.

Adenosine Triphosphate↗
PubMed1975

[Certain characteristics of myocardial metabolism in long-term experimental hypotension and the effect of administration of adenosine triphosphate and fructose 1,6-diphosphate].

Several indices of energy exchange and protein-amino acid metabolism in the myocardium were studied experimentally in dogs subjected to long-term hypotension (Wiggers' technique, arterial pressure of 40 mm Hg for 3 hours). It was established that by the end of the fixed period of hypotension the myocardial content of adenosine triphosphate, creatinephosphate, glycogen decreased significantly, while the amount of nonorganic phosphorus, lactic and pyruvic acids increased. At the same time the content of watersoluble protein fraction and of most of the 18 identified amino asids decreases in the cardiac muscle. Fractionated intravenous injections of adenosine triphosphate or 1,6-diphosphate fructose permitted to prevent the development of energy deficit, and, to a great extent, that of protein-amino acid metabolism disorders in dogs subjected to long-term hypotension.

Adenosine Triphosphate↗
PubMed1969

The re-distribution of cytochrome oxidase, noradrenaline and adenosine triphosphate in adrenergic nerves constricted at two points.

1. The experiments correlate certain changes in the ultrastructure of cat hypogastric nerves constricted at two points with the distribution of a mitochondrial enzyme (cytochrome oxidase), noradrenaline (stored in some of the vesicles with an electron dense core, i.e. granular vesicles) and adenosine triphosphate (ATP) (present in noradrenaline storage granules, mitochondria and the soluble fraction of the axon).2. Noradrenaline (NA) and granular vesicles accumulated proximal but not distal to both constrictions. The total amount of NA and the concentration of granular vesicles above the first constriction was greater than that present in a similar piece of normal nerve, indicating that the cell body was continuing to produce the transmitter despite injury to its axon. The granular vesicles proximal to the first constriction were found in swollen or distorted axons and in new axonal outgrowths. It was concluded that the movement of NA in these constricted nerves was only centrifugal in direction.3. Mitochondria and cytochrome oxidase accumulated on both sides of the two constrictions, indicating a bi-directional movement of mitochondria in the damaged axons. The possibility that some of the increase in the cytochrome oxidase could be related to an increase in the number of mitochondria in cells other than neurones is considered.4. The adenosine triphosphate content increased on both sides of the two constrictions. This increase developed more slowly and was less marked than that of the other two substances.5. It was concluded that (a) there was a close correlation between the behaviour of noradrenaline and granular vesicles and between cytochrome oxidase and mitochondria, (b) the dense cored vesicles and the mitochondria moved independently of one another and at different rates after constriction of non-myelinated axons, (c) while some of the changes may be attributed to an obstruction to the free movement of axoplasm others may be due to an active reaction to axonal injury, and (d) localized intraaxonal synthesis of noradrenaline and cytochrome oxidase did not occur between the two constrictions.

Adenosine Triphosphate↗
PubMed2003

Mechanisms involved in adenosine triphosphate--induced platelet aggregation in whole blood.

OBJECTIVE: Effects on platelet aggregation of adenosine triphosphate (ATP) released from damaged cells and from platelets undergoing exocytosis have not been clearly established. In this study we report on the effects of ATP on platelet aggregation in whole blood. METHODS AND RESULTS: Aggregation, measured using a platelet-counting technique, occurred in response to ATP and was maximal at 10 to 100 micromol/L. It was abolished by MRS2179, AR-C69931, and creatine phosphate/creatine phosphokinase, implying that conversion to adenosine diphosphate (ADP) is required. ATP did not induce aggregation in platelet-rich plasma, but aggregation did occur when apyrase or hexokinase was added. Aggregation also occurred after addition of leukocytes to platelet-rich plasma (as a source of ecto-ATPase), and this was potentiated on removal of adenosine by adenosine deaminase, indicating that adenosine production modulates the response. Dipyridamole, which inhibits adenosine uptake into erythrocytes, inhibited aggregation induced by ATP in whole blood, and adenosine deaminase reversed this. DN9693 and forskolin synergized with dipyridamole to inhibit ATP-induced aggregation. CONCLUSIONS: ATP induces aggregation in whole blood via conversion of ATP to ADP by ecto-ATPases on leukocytes. This is inhibited by agents that prevent adenosine removal. Reduced aggregation at high concentrations of ATP (>100 micromol/L) may be a consequence of inhibition by ATP of ADP action at ADP receptors.

Adenosine Deaminase↗
PubMed1991

Vagal involvement in the action of exogenous adenosine triphosphate on reflex renal sympathetic nerve activity.

The reason why adenine compounds when used as hypotensive agents are devoid of significant reflex sympathetic activity, such as rebound hypertension and tachycardia, is not clearly understood. This study, performed on alpha-chloralose-anesthetized dogs, examined, first, the effects of adenosine triphosphate (ATP) and adenosine as compared with those of sodium nitroprusside on efferent renal sympathetic nerve activity (RSNA), as an indicator of general reflex sympathetic activity, and second, whether vagal involvement could be demonstrated in the action of ATP and adenosine on RSNA. Renal sympathetic nerve activity increased progressively with increasing doses of sodium nitroprusside (5, 10, and 20 micrograms/kg) and adenosine (0.5, 2.0, and 4.0 mg/kg), whereas ATP suppressed RSNA at 2.0 and 4.0 mg/kg. High doses of ATP and adenosine (4.0 mg/kg) were injected into intact (n = 7) and vagotomized dogs (n = 7). Both ATP and adenosine induced rapid onset of hypotension without rebound hypertension and tachycardia. After vagotomy, the attenuation of RSNA by ATP was completely abolished and rebound hypertension and tachycardia were observed. Vagotomy did not alter the effect of adenosine on RSNA. It is concluded that ATP-induced hypotension is associated with attenuation of sympathetic efferent nerve activity mediated through vagal afferent pathways. Vagal afferent impulses are thought to be one of the mechanisms that inhibit reflex sympathetic activities, such as rebound hypertension after ATP-induced hypotension. The mechanisms by which adenosine inhibits reflex sympathetic activity are not, however, secondary to vagal afferent involvement and must be multifactorial.

Adenosine↗
PubMed1982

Antiarrhythmic and hemodynamic responses to adenosine triphosphate during infusion of epinephrine in dogs anesthetized with halothane.

The effects of adenosine triphosphate (ATP) on cardiovascular responses to epinephrine were evaluated in dogs anesthetized with halothane. The dose of epinephrine required to induce arrhythmias averaged 1.05 +/- 0.52 microgram/kg/min. The dose of ATP required to abolish these arrhythmias averaged 1.64 +/- 0.67 mg/kg/min. ATP had not only an antiarrhythmic effect but also antagonized epinephrine-induced increases in heart rate, systemic vascular resistance, mean arterial blood pressure, and further increased cardiac index. ATP had, however, no significant effect on epinephrine-induced increases in myocardial contractility.

Adenosine Triphosphate↗
PubMed1983

Adenosine triphosphate in human semen: a quantitative estimate of fertilizing potential.

The concentration of adenosine triphosphate (ATP) per milliliter of ejaculate was found to be significantly correlated with the following parameters: sperm concentration, number of motile spermatozoa per milliliter, capacity of spermatozoa to migrate against gravity, and in vitro potential to penetrate zona-free hamster ova. The ATP concentration was significantly lower in the semen of infertile men with normal sperm concentration and motility, compared with matched fertile donors. The ATP concentration of deep-frozen donor semen was significantly correlated with its fertilizing potential as estimated from the pregnancy per cycle index in an artificial insemination by donor semen program. These qualities suggest that measurement of semen ATP may be a possible biochemical method for the quantitation of the actual fertilizing potential of the ejaculate.

Adenosine Triphosphate↗
PubMed1979

Comparison of Reductions in Adenosine Triphosphate Content, Plasma Membrane-associated Adenosine Triphosphatase Activity, and Potassium Absorption in Oat Roots by Diethylstilbestrol.

The possibility was investigated that diethylstilbestrol (DES) inhibits potassium absorption in oat (Avena sativa L. cv. Goodfield) roots by inhibiting mitochondrial functions in addition to inhibiting the plasma membrane ATPase. DES at 10(-6) molar stimulated the mitochondrial ATPase slightly, but higher concentrations had no effect. Oxidative phosphorylation by isolated mitochondria was inhibited 50% by 2.6 x 10(-5) molar DES; concentrations of 10(-4) molar or greater were completely inhibitory. After a lag of about 2 minutes, 10(-4) molar DES produced a linear decrease in ATP content of excised roots. After 20 minutes, the ATP content of the tissue was about 50% of the control and remained at that level after 30 minutes in DES.Comparison of changes in ATP content, plasma membrane ATPase activity, and K(+) absorption rate with time in the presence of DES showed that the rapid decrease in K(+) absorption rate corresponded more closely with the decrease in ATPase activity than the decrease in ATP content. Total inhibition of the ATPase was calculated by multiplying together the percentage decreases in ATPase activity and ATP content. At times greater than 10 minutes this "net" ATPase activity corresponded very closely with the K(+) absorption rate.These results show that DES can inhibit potassium absorption by reducing mitochondrial ATP production in addition to inhibiting the plasma membrane ATPase. However, the rapid (less than 5 minutes) inhibition of absorption is caused by direct inhibition of the ATPase rather than a reduced ATP supply because the ATP content is lowered only slightly whereas the ATPase is inhibited dramatically in that time. The relationship between plasma membrane ATPase activity and K(+) absorption rate as inhibited by DES supports the hypothesis that the ATPase is involved in cation absorption by plant roots.

Journal Article↗