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The decrease of neuromuscular transmission by adenosine depends on previous neuromuscular depression.

J A Ribeiro

    Archives Internationales De Pharmacodynamie Et De Therapie
    |January 1, 1982
    PubMed
    Summary
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    Adenosine amplifies neuromuscular blockade by tubocurarine or altered ion concentrations, but not tetrodotoxin. This suggests adenosine acts postsynaptically or presynaptically to inhibit neuromuscular transmission.

    Area of Science:

    • Neuroscience
    • Pharmacology

    Background:

    • Adenosine is a neuromodulator present at the neuromuscular junction.
    • Its precise role in modulating neuromuscular transmission under blockade conditions is not fully understood.

    Purpose of the Study:

    • To investigate the action of adenosine on neuromuscular transmission during blockade.
    • To determine the sites of action for adenosine's inhibitory effects.

    Main Methods:

    • Studied neuromuscular transmission in the presence of adenosine (0.5 mM) and various blocking agents: tubocurarine, tetrodotoxin, and high Mg2+/low Ca2+ solutions.
    • Examined the effects of adenosine at different temperatures (room temperature and 37°C).

    Main Results:

    • Adenosine enhanced the inhibitory effects of tubocurarine, high Mg2+, and low Ca2+.

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  • The potentiation by adenosine was dependent on the degree of existing neuromuscular inhibition.
  • Adenosine's effects varied with temperature, showing greater inhibition at room temperature with tubocurarine but higher potency at 37°C with ionic blockade.
  • Adenosine did not alter the effects of tetrodotoxin.

    • Conclusions:

    • Adenosine's inhibitory action requires partial neuromuscular blockade, suggesting postsynaptic (ACh receptor blockade) or presynaptic (reduced transmitter release) mechanisms.
    • Endogenous adenosine may play a role in conditions affecting neuromuscular transmission, such as myasthenia gravis.