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Results for “ADENOSINE TRIPHOSPHATE”

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At least 19 recordsLinked to original sources

PubMed1983

Effect of adenosine, adenosine triphosphate, adenosine deaminase, dipyridamole and aminophylline on acetylcholine release from electrically-stimulated brain slices.

The effect of adenosine on release of acetylcholine (ACh) was investigated in slices of rat cortex perfused with Krebs solution, at rest and during electrical stimulation at frequencies between 0.2 and 20 Hz. Electrical stimulation brought about a linear increase in release of ACh. Adenosine, in concentrations ranging from 1 to 100 microM, reduced in a dose-dependent manner the release of ACh and was more active on the stimulated than on the resting release. However, the fractional reduction by adenosine of stimulated release of ACh did not vary with increasing stimulation rate. Adenosine triphosphate was less active than adenosine in reducing release of ACh. The inhibitory effect of adenosine was antagonized by aminophylline (0.5 mM) and did not occur when the stimulated release of ACh was enhanced by blocking muscarinic autoreceptors with atropine (15 nM). Aminophylline (0.1 and 0.5 mM) itself exerted a biphasic effect on release of ACh, increasing it at rest and during stimulation at low frequencies, and decreasing it at higher stimulation rates. The manipulation of endogenous adenosine concentrations by adding adenosine deaminase or diphyridamole, an inhibitor of adenosine uptake, had little effect on release of ACh. Dipyridamole, (4 microM), only significantly decreased release of ACh at the 20 Hz stimulation rate.

Acetylcholine↗

PubMed1985

Responses evoked by electrical stimulation, adenosine triphosphate, adenosine and 4-aminopyridine in taenia caeci of the guinea-pig.

Electrical stimulation of the guinea-pig taenia caeci (5 Hz, 2 s) caused enhancement of the [3H]purine flux from [3H]adenosine pools, accompanied by hyperpolarization (inhibitory junction potential) and relaxation of the muscle cells (35 degrees C). Interaction with receptors sensitive to catecholamines and acetylcholine was prevented by phentolamine (10(-6)M), propranolol (10(-6)M) and atropine (10(-6)M, respectively. The hyperpolarization and relaxation were completely inhibited by tetrodotoxin (TTX; 3 X 10(-7)M) but a substantial part of the [3H]purine flux persisted. The flux from the [3H]purine pool, from the [3H]methylcholine pool and from the noradrenaline pool was enhanced in the presence of 4-aminopyridine (3 X 10(-4)M; 4-AP), known to facilitate transmitter release. The release from the [3H]methylcholine pool was limited by hemicholinium (HC-3; 5 X 10(-4) M) and the release of noradrenaline was limited by reserpine (5 mg/kg; 24 h). The excess release of [3H]purine caused by 4-AP was completely abolished in the presence of TTX in preparations treated with HC-3 and reserpine. Addition of 4-AP to the Krebs solution evoked contraction of the smooth muscle cells. This response was abolished in the presence of HC-3 or atropine. The relaxation was also observed in reserpinized preparations in the presence of HC-3 and was not inhibited by either phentolamine or propranolol but was abolished in the presence of TTX. Hyperpolarization and suppression of spike activity accompanied the relaxation induced by 4-AP in reserpinized preparations treated with HC-3. Comparable responses were evoked by electrical stimulation of taenia caeci, by adenosine triphosphate (4 X 10(-4) M; ATP) and by adenosine (4 X 10(-4) M) in these experimental conditions. These responses evoked by electrical stimulation and by ATP were reversed in the presence of apamin (3 X 10(-7) M); the effect was reflected by an increased spike activity and contraction of the muscle cells in contrast to the adenosine response.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗

PubMed1994

Primary cultures of bovine inner zone adrenocortical cells secrete cortisol in response to adenosine triphosphate, adenosine diphosphate, and uridine triphosphate via a nucleotide receptor which may be coupled to two signal generation systems.

Cultured inner zone cells isolated from bovine adrenal cortex secreted cortisol in a dose-dependent fashion in response to ATP and ADP. The threshold response was at 10(-6) M ATP, reaching a maximum by 10(-4) M ATP, at which concentration the n-fold relative to basal was 43.8 +/- 22.3 (mean +/- SD, n = 3). The response to 10(-4) M ATP remained linear for up to 2 h, and the cells appeared morphologically normal after removal of the stimulus. Stimulation of cortisol secretion by ATP was evident after 24 h in primary culture and reached a maximum after 48-72 h, thereafter declining. No response was detected in freshly isolated cells. The possibility that added ATP was degraded over the course of the incubation was investigated by separating ATP, ADP, AMP, and adenosine by high resolution anion exchange chromatography after different times of exposure to the cells. Although there was degradation--largely to ADP--about 50% of the ATP remained at 1 h. The potency order of a range of purines was as follows: ATP = ADP > 2-methyl-S-ATP > alpha, beta-methylene ATP = beta, alpha-methylene ATP = AMP. Cells were also responsive to the pyrimidine nucleotide uridine 5'-triphosphate, which was equipotent with ATP. The purinergic antagonist suramin was relatively ineffective. Cells grown in the presence of [3H]inositol (10 microCi/ml) for 48 h (to prelabel the membrane phosphoinositide pool to isotopic equilibrium) showed a time- and dose-dependent increase in [3H]inositol-labeled total phosphoinositols in response to ATP or ADP; the response was linear for at least 60 min. Cells labelled with the Ca2+ indicator fura-2 showed an increase in intracellular calcium in response to 10(-4) M ATP on days 3 and 4 of culture. Basal intracellular Ca2+ was found to be 57.3 +/- 39.3 nmol/liter (mean +/- SD, n = 12 cell suspensions) rising to 171 +/- 84 nmol/liter (mean +/- SD, n = 12 cell suspensions) in response to ATP (10(-4) M). In response to ATP, bovine inner zone cells also demonstrated a dose-dependent increase in intracellular cAMP measured after 1 min stimulation. It was not possible to account for the cAMP response on the basis of conversion of ATP to adenosine, which then acted at an A2 receptor.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Diphosphate↗

PubMed1985

The influence of adenosine triphosphate, adenosine diphosphate and cytochalasin B on nucleotide exchange of F-actin. Evidence that treadmilling is not involved.

[14C]ATP-containing G-actin was polymerized to [14C]ADP-containing F-actin. The exchange of the filament-bound nucleotide with nucleotides of the medium was investigated by measuring the loss of radioactivity from the filaments under various conditions. Nucleotide exchange was faster in the presence of ATP than of ADP (this could be observed in the presence of Mg2+ as well as in the presence of Ca2+). Cytochalasin B had a small accelerating effect in the presence of ATP but had no effect in the presence of ADP. The kinetics of exchange remained unchanged when the filaments contained a 'cap' of actin with non-radioactive nucleotides, suggesting that nucleotide exchange was not a property of the filament ends.

Actins↗

PubMed1980

Electrochemical proton gradient across the cell membrane of Halobacterium halobium: effect of N,N'-dicyclohexylcarbodiimide, relation to intracellular adenosine triphosphate, adenosine diphosphate, and phosphate concentration, and influence of the potassium gradient.

The proton motive force across the cell membrane of halobacterial cells has been estimated and compared to intracellular values of ATP, ADP, and inorganic phosphate concentrations with respect to the chemiosmotic hypothesis. The accumulation of 14C-labeled indicator substances, triphenylmethylphosphonium for the membrane potential and 5,5-dimethyloxazolidine-2,4-dione for the pH difference between the cell interior and the medium, has been measured in the cells. Values up to 270 mV for the proton motive force have been found in cells pretreated with N,N'-dicyclohexylcarbodiimide (DCCD, 10(-4) M, 30 degrees C, 12 h). Upon illumination a high membrane potential is generated, which is then gradually replaced by a large pH difference. Cells treated with lower DCCD concentrations show only an enhancement of membrane potential upon illumination; the pH difference remains at a low level. Under anaerobic dark conditions, untreated cells maintain a proton motive force of 120-140 mV, which is equilibrated with the intracellular levels of ATP, ADP, and inorganic phosphate. The pH gradient is 1 unit at pH 6 but 0 at pH 8. The membrane potential is low (60-80 mV) at pH 6 and high (120-130 mV) at pH 8. We propose that the proton translocating ATPase compensates for the lowered pH difference at high external pH values by enhancing the membrane potential. The concentration difference of the potassium ions influences the proton motive force and the intracellular ATP levels, apparently via its action on the membrane potential. When the difference of the chemical potential of the potassium ion, expressed in millivolts, exceeds the preexisting membrane potential, the intracellular ATP level is enhanced. When the difference of the chemical potential of the potassium ion (millivolts) is smaller than the membrane potential, the ATP level is decreased.

Adenosine Diphosphate↗

PubMed1972