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Browsing by Author "VARAGIć, V.M. (7006591279)"

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    THE EFFECT OF 5‘‐N‐ETHYLCARBOXAMIDEADENOSINE ON THE ISOLATED HEMIDIAPHRAGM OF THE RAT DURING DIRECT AND INDIRECT ELECTRICAL STIMULATION
    (1989)
    PROSTRAN, M. (7004009031)
    ;
    VARAGIć, V.M. (7006591279)
    Summary— Similar to adenosine and some of its derivatives, 5′‐N‐ethylcarboxamideadenosine (NECA) produced a biphasic effect on the isolated hemidiaphragm of the rat: a potentiation of the isometric contraction during direct electrical stimulation (in the presence of dipyridamole), and a depression during indirect electrical stimulation, and particularly so in a partially curarized preparation. The potentiating effect is presumed to be due to activation of the cAMP system, probably through A2 receptor sites, although a differentiation of the receptor subtype could not be made with aminophylline and XAC. Inhibition is most probably due to a depressant action of NECA on the acetylcholine release from the motor nerve terminals. These results accord with our previous findings, suggesting that adenosine may be part of a buffer system which participates in balancing the excitatory and inhibitory influences on skeletal muscle contraction. 1989 Société Française de Pharmacologie et de Thérapeutique
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    Publication
    THE EFFECT OF 5‘‐N‐ETHYLCARBOXAMIDEADENOSINE ON THE ISOLATED HEMIDIAPHRAGM OF THE RAT DURING DIRECT AND INDIRECT ELECTRICAL STIMULATION
    (1989)
    PROSTRAN, M. (7004009031)
    ;
    VARAGIć, V.M. (7006591279)
    Summary— Similar to adenosine and some of its derivatives, 5′‐N‐ethylcarboxamideadenosine (NECA) produced a biphasic effect on the isolated hemidiaphragm of the rat: a potentiation of the isometric contraction during direct electrical stimulation (in the presence of dipyridamole), and a depression during indirect electrical stimulation, and particularly so in a partially curarized preparation. The potentiating effect is presumed to be due to activation of the cAMP system, probably through A2 receptor sites, although a differentiation of the receptor subtype could not be made with aminophylline and XAC. Inhibition is most probably due to a depressant action of NECA on the acetylcholine release from the motor nerve terminals. These results accord with our previous findings, suggesting that adenosine may be part of a buffer system which participates in balancing the excitatory and inhibitory influences on skeletal muscle contraction. 1989 Société Française de Pharmacologie et de Thérapeutique

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