Adenosine-dependent formation of cyclic AMP in brain slices

Mah, Heduck; Daly, John W.

doi:10.1016/0031-6989(76)90030-8

Cited by 147 publications

(44 citation statements)

References 24 publications

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“…In fact, neither of the excitatory amino acids activate adenylate cyclase activity in a cell free system from the hipppocampus under any conditions. As has been suggested (35,36), the stimulated formation of cAMP by 25,26,39). At present, the biochemical and pharmacological qualifications of ,"CSA neurones" are not clear.…”

supporting

confidence: 55%

Neurochemical characterization of cysteine sulfinic acid, an excitatory amino acid, in hippocampus.

Baba

1987

Jpn.J.Pharmacol

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supporting

confidence: 55%

Neurochemical characterization of cysteine sulfinic acid, an excitatory amino acid, in hippocampus.

Baba

1987

Jpn.J.Pharmacol

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“…This shorter duration is readily explained by the uptake and metabolism of adenosine, but not of the other analogues (Mah & Daly, 1976).…”

Section: Ion Studiesmentioning

confidence: 91%

“…This is further evidence for an action on an extracellular receptor since intracellular actions of adenosine would be prevented by an uptake blocker. In addition, since the adenosine analogues do not share the adenosine uptake mechanism sensitive to dipyridamole, (Mah & Daly, 1976), it is not surprising that this drug does not alter the concentration-response curves of the analogues. In addition, we have shown that the termination of the action of the analogues is not dependent on an uptake process in the smooth muscle system studied here.…”

Section: Ion Studiesmentioning

confidence: 99%

Evidence that the P₁‐purinoceptor in the guinea‐pig taenia coli is an A₂‐subtype

Burnstock

Hills

Hoyle

1984

British J Pharmacology

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1 The effects of 5'-N-ethylcarboxamidoadenosine (NECA), L-NECA, 2-chloroadenosine, N6-phenylisopropyladenosine (L-PIA and D-PIA), cyclohexyladenosine (CHA), and adenosine were examined on the guinea-pig taenia coli. 2 All the analogues except L-NECA caused relaxations; the order of potency for the series was:3 L-PIA was twice as potent as D-PIA in inducing relaxations of the guinea-pig taenia coli. 4 Adenosine and its analogues that induce relaxation all caused a slow membrane hyperpolarization; differences in the rates of hyperpolarization and latencies were apparent, although not statistically significant. 5 The duration of the response to adenosine was significantly less than that for any adenosine analogue. 6 Ion studies, using the sucrose gap, revealed that responses to the analogues were attenuated in elevated extracellular potassium or reduced extracellular chloride. 7 8-Phenyltheophylline, a potent P1-purinoceptor antagonist, caused a rightward shift of all the adenosine and analogue concentration-response curves. 8 Dipyridamole, an adenosine uptake inhibitor, potentiated the relaxations to adenosine but had no significant effect on the relaxations induced by the analogues. 9 It is concluded that NECA, 2-chloroadenosine, L-PIA, CHA, D-PIA and adenosine mediate their relaxant effects via an extracellular P1-purinoceptor which displays characteristics of the A2-subtype as determined by the rank order of agonist potency. Electrophysiological analysis of the responses to each of the analogues did not reveal any marked differences in the modes of action even between NECA and L-PIA (preferential A2-and Al-receptor agonists, respectively).

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“…Thus, the synergistic potentiation of the anti aggregating activity of adenosine by EG626 probably did not result from an inhibition of adenosine transport and/or adenosine deaminase. This speculation is supported in part by the finding that EG626 also potentiates the antiaggregating activity of 2-chloro adenosine which is not a substrate for uptake (17,18) and adenosine deaminase (19).…”

Section: Methodsmentioning

confidence: 95%

“…6). It is well established that 2-chloro adenosine mimics adenosine action, but is not a substrate for uptake (17,18) and adenosine deaminase (19). Therefore, the effect of EG626 on the antiaggregating activity of 2-chloroadenosine was examined.…”

Section: Methodsmentioning

confidence: 99%

Potentiation of antiaggregating activity of adenosine by a phosphodiesterase inhibitor, EG626 (oxagrelate), in human platelets in vitro.

et al. 1984

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Abstract-EG626(oxagrelate), a specific inhibitor of cyclic AMP phosphodiesterase, produced in vitro a concentration-dependent inhibition of platelet aggregation induced by collagen and ADP in human platelets.When adenosine was added to the platelet rich plasma (PRP) in the presence of a threshold concentration of EG626, the potency of adenosine in inhibiting platelet aggregation was markedly potentiated.This potentiating effect of EG626 proved to be synergistic, but not additive and was accompanied by a marked accumulation of cyclic AMP in the platelets.The antiaggregating and cyclic AMP increasing activities of adenosine were little affected by S-(p-nitrobenzyl)-6-thioguanosine (6TG) , an uptake in hibitor of adenosine, or 2'-deoxycoformycin, an inhibitor of adenosine deaminase. The incorporation of adenosine into platelets was abolished by 6TG. These observations indicate that incorporation of adenosine into platelets is not required for inhibition of aggregation or an increase in cyclic AMP and that the site of action of adenosine is probably extracellular.It also appears that the synergistic action by EG626 is not the result of an inhibition of adenosine uptake and/or adenosine deaminase.This speculation is supported in part by the finding that EG626 also potentiates the antiaggregating activity of 2-chloroadenosine. Antiaggregating activity of prostaglandin E,, an activator of adenylate cyclase, was markedly poten tiated in combination with EG626.Dibutyryl cyclic AM P showed a time-dependent inhibition of the platelet aggregation, and the inhibitory action was markedly potentiated by EG626. Qualitatively similar results were obtained with another phosphodiesterase inhibitor, 3-isobutyl-1 -methylxanthine (IBMX). All these data suggest that the synergistic potentiation of the antiaggregating activity of adenosine by EG626 might be due to the synergistic accumulation of cyclic AM P in the platelets. This action is mediated through activation of adenylate cyclase by adenosine in combination with the inhibition of cyclic AMP phosphodiesterase by EG626.

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Adenosine-dependent formation of cyclic AMP in brain slices

Cited by 147 publications

References 24 publications

Neurochemical characterization of cysteine sulfinic acid, an excitatory amino acid, in hippocampus.

Neurochemical characterization of cysteine sulfinic acid, an excitatory amino acid, in hippocampus.

Evidence that the P₁‐purinoceptor in the guinea‐pig taenia coli is an A₂‐subtype

Potentiation of antiaggregating activity of adenosine by a phosphodiesterase inhibitor, EG626 (oxagrelate), in human platelets in vitro.

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Adenosine-dependent formation of cyclic AMP in brain slices

Cited by 147 publications

References 24 publications

Neurochemical characterization of cysteine sulfinic acid, an excitatory amino acid, in hippocampus.

Neurochemical characterization of cysteine sulfinic acid, an excitatory amino acid, in hippocampus.

Evidence that the P1‐purinoceptor in the guinea‐pig taenia coli is an A2‐subtype

Potentiation of antiaggregating activity of adenosine by a phosphodiesterase inhibitor, EG626 (oxagrelate), in human platelets in vitro.

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Product

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Evidence that the P₁‐purinoceptor in the guinea‐pig taenia coli is an A₂‐subtype