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PubMed1976

Inhibition of mammalian polyadenylate polymerase by 2-aza-1,N6-etheno-adenosine triphosphate.

2-Aza-1,N6-etheno-adenosine triphosphate (aza-epsilonATP), a fluorescent analog of adenosine triphosphate, significantly inhibits polyadenylate [poly(A)] polymerase of bovine lymphosarcoma and calf thymus, with 50% inhibition at 200 muM (in the presence of an equal concentration of adenosine triphosphate). Calf thymus RNA polymerases II and III are inhibited 32 and 20%, respectively, by a 3.8-fold excess of aza-epsilonATP; DNA polymerase alpha is not inhibited. The inhibition of poly(A) polymerase by aza-epsilonATP appears to be competitive with adenosine triphosphate; incorporation of aza-epsilonATP is not observed. Polymers of 2-aza 1,N6-etheno-adenosine monophosphate are used as primers, but pootly. 1,N-Etheno-adenosine triphosphate and 9-beta-D-arabinofuranosyladenine triphosphate are poor inhibitors of poly(A) polymerase; adenosine diphosphate is ineffective. Deoxyadenosine triphosphate inhibits to the same extent as aza-epsilonATP, while other naturally occurring nucleotides inhibit poly(A) polymerase to varying degrees, with deoxynucleoside triphosphates more potent than ribonucleoside triphosphates. Inhibition of poly(A) polymerase by naturally occurring nucleoside triphosphates suggests that nucleotides may regulate the enzyme in vivo; inhibition by the fluorescent analog aza-epsilonATP suggests that this compound may be useful in elucidating poly(A) metabolism in both normal and neoplastic cells.

Adenosine Triphosphate↗
PubMed1999

Acute effects of adenosine triphosphates, cyclic 3',5'-adenosine monophosphates, and follicle-stimulating hormone on cytosolic calcium level in cultured immature rat Ssertoli cells.

The ability of ATP and FSH to induce intracellular calcium [Ca(2+)](i) changes in Sertoli cells is imperfectly understood and reports are conflicting. We have applied the single-cell microfluorometry technique with the calcium probe indo-1 to investigate [Ca(2+)](i) in individual cultured Sertoli cells. When cells were exposed to ATP, cAMP, and FSH, a fast and biphasic increase in [Ca(2+)](i) was obtained in 100%, 70%, and 56% of cells, respectively. Caffeine did not activate Ca(2+) mobilization, while thapsigargin suppressed the peak response. External calcium free-EGTA buffer suppressed the plateau phase, while blockers of voltage-operated Ca(2+) channels did not abolish the response to cAMP and ATP. We conclude that the three messengers mobilized Ca(2+) from intracellular thapsigargin-sensitive stores, which induced a subsequent Ca(2+) influx from the extracellular medium by a voltage-independent Ca(2+) entry. The well-documented mechanisms by which these messengers act on cells support the idea that they release Ca(2+) from smooth endoplasmic reticulum by two different pathways, or that FSH and cAMP first release ATP, which then acts on cells. Among the cells, 77% and 80% responded, respectively, to FSH and cAMP by a delayed long-lasting decrease in [Ca(2+)](i) that was never recorded in the presence of ATP. This suggests that FSH and cAMP also promote a slow redistribution of [Ca(2+)](i) from the exchangeable pool to the bound nonexchangeable pools. Involvement of voltage-operated and voltage-independent calcium channels in the response of Sertoli cells to ATP, FSH, and cAMP is discussed.

Adenosine Triphosphate↗
PubMed1975

Formation of adenosine triphosphate from Pi and adenosine diphosphate by purified Ca-2+-adenosine triphosphatase.

Ca-2+-ATPase purified from sarcoplasmic reticulum of rabbit muscle forms a phsophoeznyme when exposed to inorganic phosphate in the presence of Mg-2+. On addition of ADP and Ca-2+ virtually all of the phosphate bound to the enzyme is transferred to form ATP. It has been shown previously and confirmed by us that (a) the purified ATPase contains one major polypeptide and about 30% phospholipids; (b) on removal of residual detergent by passage through Sephadex the enzyme forms vesicular membranes; and (c) these vesicles are leaky and incapable of accumulating Ca-2+. Our findings therefore indicate that we have observed ATP generation from ADP and P-i without the formation of an ion gradient across a membrane. We propose that the energy derived from ion-protein interaction drives the formation of ATP.

Adenosine Diphosphate↗
PubMed1985

The hypotensive effect of intracarotid injections of adenosine triphosphate depends on its hydrolysis to adenosine.

The effects of intra-carotid injections of adenosine, adenosine triphosphate (ATP) and alpha-beta-methylene ATP were studied on arterial blood pressure of anaesthetized cats. Adenosine and ATP decreased arterial blood pressure, whilst the ATP stable analogue, alpha-beta-methylene ATP caused a dose-dependent increase in arterial blood pressure. These results suggest that the hypotensive action of ATP might depend on its previous hydrolysis into adenosine.

Adenosine↗
PubMed1998

Preparation of liposome-encapsulating adenosine triphosphate.

Liposomes encapsulating adenosine triphosphate (ATP) were prepared by sonication, and the liposomes were evaluated for use in a drug delivery system. The liposomes, which were composed of phosphatidylcholine and cholesterol, were about 1.1 microm in size, as observed under a microscope. From their size, the vesicles were thought to be multilamellar. The maximum concentration of ATP in the liposomes was 1.0 mM, when the initial concentrations of lipid and ATP were 20 mM and 300 mM, respectively. The maximum entrapment ratio of ATP in the liposomes was 88%, when the initial concentrations of lipid and ATP were 20 mM and 500 mM, respectively. About 4% of ATP was encapsulated in these experiments. When liposomes contained 4-7% of cholesterol, about 35% of encapsulated ATP was released from the liposomes for 90 hours at 37 degrees C in vitro. These findings indicated that liposomes encapsulating ATP could be used for the treatment of ischemic retina.

Adenosine Diphosphate↗
PubMed2005

The effect of adenosine triphosphate on vecuronium-induced neuromuscular block.

Continuous IV adenosine triphosphate administration has been used during surgery in the expectation of analgesic and vasodilative effects. Because adenosine triphosphate inhibits neuromuscular transmission, we investigated whether the neuromuscular effect of vecuronium was enhanced by IV adenosine triphosphate in 29 patients randomly given either continuous IV adenosine triphosphate 0.1 mg.kg(-1).min(-1) or 0.9% NaCl when undergoing elective minor surgery. Anesthesia was induced and maintained with propofol. Neuromuscular monitoring was recorded from the adductor pollicis muscle using electromyography with train-of-four stimulation of the ulnar nerve. Vecuronium 25, 30, or 40 microg/kg was given and lag time, onset time, and maximum block were recorded. ED50 and ED95 values for each group were derived from least squares linear regression analysis. ED50 and ED95 values were 29 microg/kg and 44 microg/kg, respectively, for the adenosine triphosphate group and 26 microg/kg and 46 microg/kg, respectively, for the controls. Differences in lag time, onset time, and neuromuscular responses between the two groups were not statistically significant. A significantly larger number of patients in the adenosine triphosphate group showed hypotension (systolic blood pressure <80 mm Hg). Our results demonstrated that adenosine triphosphate 0.1 mg.kg(-1).min(-1) did not enhance the neuromuscular block induced by vecuronium.

Adenosine Triphosphate↗
PubMed1986

Biochemical studies: failure of tissue adenosine triphosphate levels to predict recovery of contractile function after controlled reperfusion.

This study tests the hypotheses that postischemic adenosine triphosphate levels are unreliable predictors of functional recovery, myocardial adenosine triphosphate concentration of less than 2 mumol/gm does not indicate irreversible damage, mitochondrial adenosine triphosphate generating capacity can be nearly normal despite low levels of tissue adenosine triphosphate and the failure to replenish adenosine triphosphate after ischemia is due to depletion of the adenosine nucleotide pool, which can be replenished partially by exogenous precursors (e.g., 5-amino-4-imidazolecarboxamide ribotide [AICAR]). Myocardial adenosine triphosphate was depleted to less than 2 mumol/gm by either global ischemia (37 degrees C aortic clamping) or regional ischemia (acute coronary occlusion). Reperfusion was either with normal blood or with substrate-enriched blood cardioplegic solution during total vented bypass. Tissue adenosine triphosphate content and mitochondrial adenosine triphosphate generating capacity were measured, and functional recovery was determined by right heart bypass function curves or regional segmental shortening (ultrasonic crystals). Hearts undergoing 15 minutes of global ischemia and normal blood reperfusion had impaired functional recovery (stroke work index = 58 +/- 5%; p less than 0.05 of control) despite adenosine triphosphate concentration greater than 2 mumol/gm. Transmural mitochondrial State 3 respiration averaged 83% of control values despite adenosine triphosphate levels of 1 mumol/gm in hearts undergoing 45 minutes of 37 degrees C global ischemia and 2 additional hours of aortic clamping with multidose glutamate-enriched blood cardioplegia. AICAR increased adenosine triphosphate to 2 mumol/gm (p less than 0.05), but functional recovery was nearly complete (stroke work index = 94 +/- 2% of control) and was comparable with and without AICAR. Hearts undergoing 4 hours of regional ischemia recovered 31 +/- 5% systolic shortening after controlled reperfusion despite tissue adenosine triphosphate less than 0.5 mmol/gm (15% of control), and they retained 63% adenosine triphosphate generating capacity. Postischemic adenosine triphosphate levels correlate poorly with functional recovery, and adenosine triphosphate levels less than 2 mumol/gm do not indicate irreversible ischemic injury. Low postischemic levels may be repleted partially by adenine nucleotide precursor supplementation (AICAR).(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1989

Dose related efficacy of adenosine triphosphate in spontaneous supraventricular tachyarrhythmias.

Intravenous adenosine triphosphate has been proved to be useful for the treatment of supraventricular tachyarrhythmias. The optimal dose to be employed, however, has yet to be stated. Forty-two episodes of spontaneous paroxysmal supraventricular tachycardia, observed in 33 patients (16 men and 17 women, mean age 51 years) were treated with intravenous boluses. These were given in 10 mg increments at increasing doses from 10 to 50 mg at intervals of three minutes if the arrhythmia persisted despite the previous dose. When using a dose less than or equal to 40 mg, tachycardia was terminated in 37 of 42 episodes in less than 50 seconds. In four of the remaining five, atrial flutter and ectopic atrial tachycardia were diagnosed after administration of adenosine triphosphate. The other patient was subsequently found to have an atrioventricular reentrant tachycardia incorporating two accessory pathways. More than half of the treated episodes of supraventricular tachycardia terminated with the minimal dose of 10 mg and 7.1% required 40 mg. In five patients, arrhythmia ceased and reappeared despite the use of adenosine triphosphate. All the patients experienced an unpleasant feeling of dyspnoea or suffocation after injection of the drug. Sinus pauses and bradycardia following termination of the arrhythmia were directly correlated with the dose employed (P less than 0.05). We conclude that adenosine triphosphate is a useful, safe and effective drug at low dose in correctly diagnosed reentrant tachycardias involving the atrioventricular node. It is also useful as a diagnostic tool in patients with supraventricular tachyarrhythmias.

Adenosine Triphosphate↗
PubMed1984

Mechanisms of adenosine triphosphate-, thrombin-, and trypsin-induced relaxation of rat thoracic aorta.

The mechanisms by which adenosine triphosphate, thrombin, and trypsin cause relaxation of vascular smooth muscle were investigated. Relaxation of the rat thoracic aorta with adenosine triphosphate, thrombin, and/or trypsin was associated with increased levels of cyclic guanosine monophosphate in both time- and concentration-dependent manners. Thrombin and trypsin did not alter cyclic adenosine monophosphate levels, whereas adenosine triphosphate increased cyclic adenosine monophosphate levels after significant relaxation occurred. Removal of the endothelium abolished adenosine triphosphate-, thrombin-, and trypsin-induced relaxation and the associated increased levels of cyclic nucleotides. Relaxation due to these agents was also inhibited by exposure to nordihydroguaiaretic acid, a lipoxygenase inhibitor, and eicosatetraynoic acid, a lipoxygenase and cyclooxygenase inhibitor. Indomethacin, a cyclooxygenase inhibitor, potentiated relaxation to these agents, whereas the increased levels of cyclic nucleotides due to adenosine triphosphate were unaltered. Bromophenacyl bromide, a phospholipase A2 inhibitor, decreased relaxation due to adenosine triphosphate, thrombin, and trypsin and the associated increased levels of cyclic nucleotides. Removal of extracellular calcium, which also presumably inhibits phospholipase A2, prevented the elevated levels of cyclic nucleotides and the inhibitory effects of adenosine triphosphate and trypsin on contraction. In contrast, sodium nitroprusside-induced relaxation and/or increased levels of cyclic guanosine monophosphate were unaltered by nordihydroguaiaretic acid, eicosatetraynoic acid, bromophenacyl bromide, and removal of extracellular calcium. After incubation of intact tissue with 32P-orthophosphate, the patterns of protein phosphorylation caused by adenosine triphosphate, thrombin, and trypsin were indistinguishable from those of acetylcholine, sodium nitroprusside and 8-bromo cyclic guanosine monophosphate. All these agents dephosphorylated myosin light chain. Thus, the present study supports the hypothesis that relaxation induced by adenosine triphosphate, thrombin, and trypsin is mediated through the formation of an endothelial factor which elevates cyclic guanosine monophosphate levels and causes cyclic guanosine monophosphate-dependent protein phosphorylation and dephosphorylation of myosin light chain.

Acetophenones↗
PubMed1987

Venodilator effects of adenosine triphosphate and sodium nitroprusside; comparisons during controlled hypotension.

Adenosine triphosphate as well as sodium nitroprusside has been used for hypotensive anesthesia. The purpose of this study was to examine the possibility that two hypotensive drugs may exert different effects on venous capacitance during controlled hypotension. In rats anesthetized with ketamine, mean arterial pressure was lowered to 50 mmHg by intravenous infusion of adenosine triphosphate or sodium nitroprusside. Venous capacitance was assessed before and during induced hypotension by measuring the mean circulatory filling pressure (MCFP). MCFP was measured after briefly arresting the circulation by inflating an indwelling balloon in the right atrium. MCFP was lower during adenosine triphosphate-induced as well as sodium nitroprusside-induced hypotension as compared with the respective value at control (P < 0.01 for adenosine triphosphate and sodium nitroprusside). However, the decrease in MCFP by adenosine triphosphate (0.8 +/- 0.1 mmHg) was less (P < 0.01) than that by sodium nitroprusside (2.3 +/- 0.3 mmHg). These results suggest that at a comparable level of arterial hypotension venodilator effect of adenosine triphosphate was less than that of sodium nitroprusside. Less venodilatation during adenosine triphosphate-induced hypotension may contribute to the maintenance of cardiac output during hypotensive anesthesia.

Journal Article↗
PubMed2002

Enhancement of cellular adenosine triphosphate levels in PC12 cells by extracellular adenosine.

To elucidate the biological significance of extracellular adenine compounds, the effects of adenosine (Ado) on cellular levels of adenine compounds, especially adenosine triphosphate (ATP), in PC12 cells were studied. Ado and inosine but not adenosine 5'-monophosphate, adenosine 5'-diphosphate, ATP, guanosine, cytosine, thymidine, and uridine, significantly enhanced cellular ATP levels in PC12 cells in time- and dose-dependent manners. Various P1 receptor agonists of Ado did not enhance the ATP level. In addition, theophylline, an antagonist of P1 receptors, did not inhibit the Ado-evoked ATP enhancement. These results suggest that the Ado receptor is not involved in the augmentation of the cellular ATP level induced by Ado in PC12 cells. The ATP-enhancing effect of Ado was potentiated by dipyridamole, an inhibitor of Ado uptake, or coformycin, an inhibitor of Ado deaminase. The effect of Ado on the ATP level was also observed when PC12 cells were incubated in glucose-free medium. Together these results suggest that enhancement of cellular ATP levels in PC12 cells by extracellular Ado might be acceleration of ATP synthesis through the Ado salvage system using hypoxanthine-guanine phosphoribosyltransferase rather than Ado kinase since 5'-iodotubercidin, an inhibitor of Ado kinase, had no effect on the enhancement elicited by Ado.

Adenosine↗