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  • 1
    Electronic Resource
    Electronic Resource
    Inhibition and excitation by adenosine in the rat hippocampus
    Amsterdam : Elsevier
    Journal of Physiology-Paris 88 (1994), S. 410 
    Details
    ISSN: 0928-4257
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0928-4257(94)90076-0
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Separation of adenosine and its derivatives by thin-layer chromatography on silica gel
    Amsterdam : Elsevier
    Journal of Chromatography A 325 (1985), S. 317-322 
    Details
    ISSN: 0021-9673
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/S0021-9673(00)96036-9
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Purinergic modulation of transmitter release
    Amsterdam : Elsevier
    Journal of Theoretical Biology 80 (1979), S. 259-270 
    Details
    ISSN: 0022-5193
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0022-5193(79)90210-8
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Involvement of α-adrenoceptors in the excitatory effect of the A2 adenosine receptors agonist 5′-N-ethylcarboxamidoadenosine (NECA) on cardiac automaticity in the isolated right ventricle of the rat (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 350 (1994), S. 632-637 
    Details
    ISSN: 1432-1912
    Keywords: Key words: Cardiac automaticity – Adenosine receptors –α-adrenoceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The effects of the non-selective A2 adenosine receptor agonist 5′-N-ethyl-carboxamidoadenosine (NECA) were studied on ventricular automaticity induced by a local injury in the isolated right ventricle of the rat. In concentrations ranging from 0.1 to 100 nM, NECA significantly increased ventricular automaticity. This effect was not apparent when the nonselective α-adrenoceptor blocker phenoxybenzamine was present at a concentration of 10 μM, which antagonizes both α1- and α2-adrenoceptors, as well as when rats were pretreated with reserpine. In non-reserpinized rats, the excitatory effect of NECA was also abolished in the presence of the selective α1-adrenoceptor antagonist prazosin, but not in the presence of the α2-adrenoceptor antagonist idazoxan. In reserpinized rats, the excitatory effect of NECA was restored in the presence of the non specific α-adrenoceptor agonist phenylephrine as well as in the presence of the selective α1-adrenoceptor agonist amidephrine but not in the presence of the selective α2-adrenoceptor agonist clonidine. These results suggest that the excitatory effect of NECA on ectopic ventricular automaticity is dependent on endogenous catecholamines and that α-adrenoceptors of type 1 are, in some way, involved in this effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169368
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  • 5
    Electronic Resource
    Electronic Resource
    Evidence that the presynaptic A2a-adenosine receptorof the rat motor nerve endings is positively coupledto adenylate cyclase (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 350 (1994), S. 514-522 
    Details
    ISSN: 1432-1912
    Keywords: Key words: CGS 21680C – Forskolin – MDL 12,330A – Rolipram – Cyclic AMP stable analogues – [3H]-Acetylcholine release – Motor nerve terminals – A2a-adenosine receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The action of the A2a-adenosine analogue, CGS 21680C, on electrically evoked [3H]acetylcholine ([3H]-ACh) release, and its interaction with forskolin (an activator of adenylate cyclase), MDL 12,330A (an irreversible inhibitor of adenylate cyclase), rolipram (an inhibitor of cyclic AMP specific phosphodiesterase), dibutyryl- (db-cAMP) and 8-bromo- (8-Br-cAMP) cyclic AMP analogues (substances that mimic intracellular actions of cyclic AMP), were investigated using rat phrenic nerve-hemidiaphragm preparations.   CGS 21680C facilitated [3H]-ACh release. Forskolin (but not 1,9-dideoxy forskolin), rolipram, db-cAMP and 8-Br-cAMP also increased evoked neurotransmitter release in a concentration-dependent manner. When the evoked [3H]-ACh release that is dependent on stimulation of the adenylate cyclase/cyclic AMP transduction system was supramaximally stimulated by these compounds, CGS 21680C (3 nmol/l) could not further increase [3H]-ACh release. Phosphodiesterase inhibition with low concentrations (≤30 μmol/l) of rolipram significantly potentiated the augmenting effect of CGS 21680C (1 nmol/l) on evoked [3H]-ACh release. MDL 12,330A (an irreversible inhibitor of adenylate cyclase) decreased evoked [3H]-ACh release. The irreversible blocking action of MDL 12,330A on [3H]-ACh release was overcome by by-passing cyclase activation with db-cAMP and 8-Br-cAMP, but could not be overcome with FSK or CGS 21680C. The inhibitory effect of MDL 12,330A on evoked [3H]-ACh release was not mimicked by nifedipine.   It is concluded that the increase in [3H]-ACh release caused by CGS 21680C results from activation of an A2a-adenosine receptor positively linked to the adenylate cyclase/cyclic AMP system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00173021
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    Paper (German National Licenses)
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