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The relationship between 5-hydroxytryptamine and adenosine triphosphate in blood platelets.

In normal platelets a proportionality was found between the amount of adenosine triphosphate (ATP) and amount of 5-hydroxytryptamine (5-HT) in platelets both before and after incubating them in plasma to which 5-HT had been added. In patients receiving reserpine and in others with myeloid leukaemia, the amount of 5-HT in the platelets and the uptake of 5-HT by them were depressed, while the amount of ATP was normal. The possibility that ATP is involved in the accumulation of 5-HT by platelets is discussed.

Adenosine Triphosphate↗

Adenosine triphosphate content in the cat carotid body under different arterial O2 and CO2 conditions.

The adenosine triphosphate (ATP) level in the carotid body has often been discussed as the crucial step in the chemoreceptive process. Therefore, the ATP level of the cat carotid body was investigated with the aid of the bioluminescence method under different stimulation conditions. Under normoxic conditions an ATP level of about 0.087 nmol/glomus was measured, which is very low in comparison to other organs. The level did not change significantly, neither under hypoxic nor hypercapnic conditions. From these results we conclude that the primary effect of the chemoreceptive process in the carotid body cannot be explained by changes of the ATP level under different stimulation conditions.

Adenosine Triphosphate↗

Evaluation of the adenosine triphosphate test in the diagnosis of urinary tract infection.

Determination by bioluminescence of the bacterial adenosine triphosphate (ATP) level in urine was evaluated as a method for detection of bacteriuria in 1126 women with symptoms of UTI and 530 attending for follow-up. Conventional urine culture was used as reference method. The criterion for bacteriuria was growth of greater than or equal to 10(5) cfu/ml, giving a prevalence of 0.60. ATP levels of less than 10 nmol/l and greater than 50 mmol/l indicated abacteriuria and bacteruiria, respectively, whereas intermediate concentrations required culture if the nitrite test was negative. With this diagnostic strategy the sensitivity and specificity was 0.96 and 0.90 at the first visit and 0.90 and 0.98 at follow-up. With some methodological improvement the ATP test could be useful in medium-sized and small laboratories.

Adenosine Triphosphate↗

[Rapid determination of bactericidal kinetics by evaluating intracellular adenosine-triphosphate in bioluminescence].

Killing kinetics measurement is usually time-consuming and tedious. Bioluminescent adenosine-triphosphate (ATP) assay, after intracellular nucleotide release by bacterial lysis, selects very quickly normal from antibiotic-modified and dead bacteria. Two simultaneous assays are performed with more and less strong lysis reagents (nucleotide releasing bacterial NRB, nucleotide releasing somatic NRS, Lumac). Bioluminescence produced in a luciferine - luciferase system is measured with Biocounter M 2010 luminometer. Differential values of two assays reflect the intracellular ATP fraction of strongest bacteria in tested cultures. Killing curves of some beta lactamines (aminopenicillin and cephalosporins) were studied with active Escherichia coli and Streptococcus pneumoniae cultures. Bactericidal action was seen within few hours, and similar variations of intracellular ATP fraction and numbers of colony-forming units obtained by reference method were observed. This method, well-suited to large series of assays and very rapid (intracellular ATP assay within one minute), performs detailed killing kinetics in real time.

Adenosine Triphosphate↗

[Effects of adenosine triphosphate on the postrotatory nystagmus and disorders of vestibular function (author's transl)].

Effects of adenosine triphosphate (ATP) on the postrotatory-induced nystagmus in rabbits and disorders of vestibular function induced by repeated administration of streptomycin in guinea pigs were studied. ATP-2Na exerted little influence on the postrotatory nystagmus in doses of 3 and 10 mg/kg, i.v., while slight suppressive effects were noted with a dose of 30 mg/kg. On the other hand, diphenidol hydrochloride remarkably suppressed the postrotatory nystagmus in a dose of 3 mg/kg i.v.. The disturbance in vestibular function following administration of streptomycin sulfate (400 mg/kg i.m., once daily x 9) was significantly alleviated when concomitant treatment with ATP-2Na (3 mg/kg i.p., 10 mg/kg i.p. and 100 mg/kg p.o., once daily x 14) or diphenidol hydrochloride (50 mg/kg p.o., once daily x 14) was given. ATP as well as diphenidol alleviated disorders in the vestibular function, while ATP had little influence on vestibular function in intact animals.

Adenosine Triphosphate↗

Generation of inorganic pyrophosphate from extracellular adenosine triphosphate by human serum and plasma.

OBJECTIVE: To quantify inorganic pyrophosphate (PPi) production from extracellular adenosine triphosphate (ATP) by human serum or plasma. METHODS: Serial measurements of ATP hydrolysis (t1/2) were performed by the luciferase method from a starting concentration of 1 microM in serum or platelet-poor plasma incubated under physiologic conditions. ATP was then pumped into another sample of each specimen using the rate constant derived from the ATP t1/2 of that specimen. Trace (32P) gamma ATP was added at the start of the infusion; conversion to (32P) inorganic orthophosphate (Pi) and to (32P) PPi was determined by precipitation of Pi as reduced phosphomolybdate before and after treatment with yeast pyrophosphatase. RESULTS: ATP was hydrolyzed by all serum and plasma specimens; the rate of hydrolysis in serum and plasma from the same blood sample was nearly identical. PPi was the major product, averaging 71%. CONCLUSION: PPi is the major product of ATP catabolism in serum and platelet-poor plasma.

Adenosine Triphosphate↗

Diurnal variation in melatonin effect on adenosine triphosphate and serotonin release by human platelets.

The effect of the pineal hormone melatonin on adenosine diphosphate-induced human platelet aggregation and adenosine triphosphate release was assessed in platelet-rich plasma obtained from normal volunteers at 08.30 and 20.30 h. In 10(-7)-10(-5) mol/l concentrations melatonin inhibited ADP-induced platelet aggregation only in the evening (p less than 0.05). ADP-induced ATP release, an index of platelet secretory processes, showed a generally greater, dose-dependent inhibition after adding melatonin (10(-9)-10(-5)mol/l) at 20.30 h as compared with 08.30 h. The inhibitory activity of melatonin (10(-9)-10(-5) mol/l) on [3H]serotonin release elicited by thrombin in washed human platelets obtained from normal volunteers was dose-dependent; the effect was generally greater at 20.30 h. The activity of the potent platelet anti-aggregating agent prostacyclin did not exhibit diurnal differences with respect to impairing ADP-induced platelet-rich plasma aggregation. These results indicate the existence of a diurnal variation of sensitivity to melatonin in human platelets.

Adenosine Diphosphate↗

Mechanisms of enhanced canine subendocardial perfusion. A comparison of adenosine triphosphate and sodium nitroprusside.

The purpose of these experiments was to determine the effects of adenosine triphosphate (ATP) and sodium nitroprusside, two compounds used to produce controlled hypotension during surgery, on regional myocardial blood flow. Intracoronary drug infusions in open chest, anesthetized dogs were used to study the direct actions of these agents on the coronary circulation as well as to avoid systemic hemodynamic effects. The actions of the endothelium-dependent and -independent vasodilators, ATP and nitroprusside, respectively, were studied before and after administration of quinacrine (an inhibitor of phospholipase A2), which blocks formation and/or release of endothelium-derived relaxing factor (EDRF). Both vasodilators produced significant increases in transmural blood flow of the drug-perfused zone. Only ATP, the endothelium-dependent vasodilator, altered the distribution of myocardial blood flow. Perfusion to the subendocardium was preferentially increased by ATP, resulting in an increase in the subendocardial-to-subepicardial flow ratio. Quinacrine markedly inhibited the increase in endo/epi produced by ATP without changing total flow. These data suggest that ATP increases total coronary blood flow by a mechanism that is independent of EDRF, but the selective redistribution of blood flow to the subendocardium is dependent on EDRF. Nitroprusside, an endothelium-independent vasodilator, produces no redistribution of myocardial blood flow.

Adenosine Triphosphate↗

Comparison of the resazurin test, adenosine triphosphate in semen, and various sperm parameters.

The results of the resazurin test (RES) and adenosine triphosphate (ATP) concentration in semen, measured by two methods, were compared for their ability to predict sperm parameters of semen samples from 42 subfertile men as assessed by a semi-computerized system. The highest correlation of RES grade was with sperm concentration (r = 0.70, P < 0.001), concentration of motile spermatozoa, concentration of motile spermatozoa with normal morphology and the ATP concentration using the reference LKB method (all r = 0.65, P < 0.001). The RES test has a positive predictive value of 93% for a progressive motile sperm concentration of 20 x 10(6)/ml or more, and a negative predictive power of 90% for the same variable at a criterion value of 10 x 10(6)/ml. The results of ATP measurement using the reference LKB and FireZyme methods presented a strong correlation (r = 0.74, P < 0.001). The correlations between ATP measurements from the FireZyme method and sperm characteristics were better than those obtained using the reference LKB method for ATP determination. It is concluded that the RES test can be performed with a relatively small volume of semen; it is easy to perform and requires not technical equipment. The accuracy and predictive value of this test are similar to more sophisticated ATP measurements. In addition, the RES may identify a subgroup of subfertile men with a decreased reducing capacity of semen.

Adenosine Triphosphate↗

Comparison of pulmonary and systemic effects of adenosine triphosphate in chronic obstructive pulmonary disease--ATP: a pulmonary controlled vasoregulator?

During stepwise incremental intravenous adenosine triphosphate (ATP) infusion, systemic and pulmonary vascular effects were compared in 10 patients with stable chronic obstructive pulmonary disease (COPD). Pulmonary vasodilation was: 1) predominant and maximal as early as the lowest dose infusion (0.1 mumol.kg-1.min-1) with pulmonary arterial mean pressure (Ppa) (-16%; p less than 0.01) and pulmonary vascular resistance (PVR) decreases (-28%; p less than 0.005) and simultaneous increasing delta PVR/delta SVR ratio; 2) associated with worsening hypoxaemia (-14%; p less than 0.001), but also with increasing alveolar-arterial oxygen pressure difference (P(A-a)O2) and venous admixture (Qs/Qt) suggesting some inhibition of hypoxic pulmonary vasoconstriction. Systemic vasodilation was: 1) clearly dose-dependent, but only reached significant level at 0.2 mumol.kg-1.min-1 with systemic arterial mean pressure (Psa) (-12.5%; p less than 0.05) and systemic vascular resistance (SVR) decreases (-30%; p less than 0.01); 2) associated with arterial carbon dioxide tension (PaCO2) decrease (-12.5%; p less than 0.005) and recurring uncontrollable hyperpnoea, suggesting a ventilatory stimulatory effect of ATP in man. In patients with stable COPD, ATP infusion has dual acute haemodynamic effects depending on the dose-level. The predominant pulmonary vasodilating effect occurs as early as the lowest dose-levels without any further increase of pulmonary vasodilation. This contrasts with the dose-related systemic vasodilation effect. Such a dual haemodynamic effect is an indirect indication of in vivo lung metabolism of ATP.

Adenosine Triphosphate↗

Effects of adenosine triphosphate on wide QRS tachycardia. Analysis in 18 patients.

A few studies have indicated that adenosine terminated triggered-activity idiopathic ventricular tachycardia, but all involved a small number of cases. The effects of adenosine triphosphate (ATP) on wide QRS tachycardia have thus not yet been completely clarified. This retrospective study was performed to evaluate the therapeutic and diagnostic utility of ATP in wide QRS tachycardia. A total of 18 patients with wide QRS tachycardia (QRS width > 120 msec, rate > or = 150 beats/min) were evaluated. ATP, 20-40 mg, was administered intravenously. An electrophysiological study and treadmill stress test were performed in all patients to elucidate the mechanism of the tachycardia. ATP terminated tachycardia or induced atrio-ventricular block in all 6 patients who had supraventricular tachycardia, but it had no effect on preexcited atrial fibrillation or pre-excited atrial flutter. Ventricular tachycardia was terminated by ATP in 5 of the 10 patients. In 4 of these 5 patients, the focus of the tachycardia was the right ventricular outflow tract. No entrainment phenomenon was demonstrated by electrophysiological study with induction of the tachycardia by stress test or isoproterenol infusion, suggesting the contribution of triggered activity to the tachycardia. In the remaining patient with complete right bundle branch block type tachycardia with right axis deviation, the mechanism of ventricular tachycardia could not be determined. In the 5 patients in whom ATP failed to terminate ventricular tachycardia, the reentry mechanism was suggested by the presence of entrainment phenomenon depicted on electrophysiological study. In summary, this study suggests that ATP terminates supraventricular wide QRS tachycardia and ventricular tachycardia due to triggered-activity, but that it has no effect on pre-excited atrial fibrillation or flutter or on ventricular tachycardia due to a reentry mechanism. These findings add to the mounting evidence regarding the therapeutic and diagnostic utility of ATP in wide QRS tachycardia.

Adenosine Triphosphate↗

THE LOCALIZATION BY ELECTRON MICROSCOPY OF HELA CELL SURFACE ENZYMES SPLITTING ADENOSINE TRIPHOSPHATE.

Cultures of normally proliferating Hela cells have been examined in thin sections by electron microscopy following glutaraldehyde fixation, staining in Wachstein and Meisel's adenosine triphosphate containing medium, postosmication, and embedding in an epoxy resin. The cells were stained in suspension in order to ensure uniform accessibility to reagents. Discrete localization of the enzyme reaction product (lead phosphate) was found at the plasma membranes of about half the cells, but nowhere else. It appeared in the form of an intensely electron-opaque deposit lying close against the outer surface of the cells and varying in amount from a chain of small particles to a dense band about 30 mmicro in width. This opaque reaction product was present over microvilli when absent elsewhere on a cell, was heaviest where microvilli and processes were profuse, and was minimal or lacking where cell surfaces were smooth. These observations are discussed in relation to both the idea that surface enzyme activity varies with the physiological phase of individual cells in a population, and the problem of how such enzyme activity becomes manifest at a given site on a morphologically changing membrane system.

Adenosine Triphosphatases↗

Effects of theophylline on the selective increases in intratumoral blood flow induced by intracarotid infusion of adenosine and adenosine triphosphate in C6 glioma-transplanted rat brains.

We have previously reported that the intracarotid administration of adenosine or adenosine triphosphate (ATP) selectively increased blood flow in intracerebrally transplanted C6 glioma cells in rats, using the hydrogen clearance method. In the present paper, we studied the difference between the effects of adenosine and ATP, using theophylline, a P1 purinoceptor blocker. The selective enhancement of the tumor blood flow by intracarotid administration of adenosine was almost totally inhibited by theophylline. In contrast, the selective enhancement by ATP was shown definitely not to be inhibited by theophylline. Therefore, it is supposed that the selective increase of intratumoral blood flow by the intracarotid infusion of adenosine is closely related to the P1 purinoceptor, and the effect of the intracarotid infusion of ATP is composed not only of the effect as degraded into adenosine but also of the effect of ATP itself.

Adenosine↗

Adenosine triphosphate inhibition of yeast trehalase.

Yeast trehalase has been found to be inhibited non-competitively by adenosine triphosphate. Such a biological control could explain the accumulation of trehalose during the stationary phase of the growth curve.

Adenosine Triphosphate↗

Hereditary hemolytic anemia with increased red cell adenosine deaminase (45- to 70-fold) and decreased adenosine triphosphate.

Hereditary hemolytic anemia, a dominantly transmitted disorder, has affected 12 family members spanning three generations. The concentration of adenosine triphosphate in the red cells was about half that of comparably reticulocyte-rich blood. Since adenosine deaminase and adenosine kinase compete for a common substrate, the greatly increased activity of the former may interfere with nucleotide salvage via the latter.

Adenine Nucleotides↗

Involvement of pertussis toxin sensitive GTP binding protein in adenosine triphosphate and thrombin-mediated responses in vascular smooth muscle cells.

Addition of thrombin (Thr) or adenosine triphosphate (ATP) to rat aortic smooth muscle cells in culture (A-10, ATCC CRL 1476) induced rapid formation of inositol phosphates and release of intracellular calcium. These responses depended on the concentration of Thr and ATP used. The Thr effect was blocked by the Thr antagonist, hirudin. ADP was almost as effective as ATP, but AMP was ineffective in mediating the effects. Pretreatment of the cells with pertussis toxin (PT) resulted in partial (60-70%) inhibition of Thr- and ATP-mediated calcium release, suggesting that in smooth muscle cells, Thr and ATP (purinergic P2) receptors are coupled to phosphoinositide specific PLC (PI-PLC) through PT-sensitive guanine nucleotide binding (G) proteins.

Adenosine Triphosphate↗