Studies on Neuromuscular Blockade by Boldine in the Mouse Phrenic Nerve-Diaphragm

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Author(s)

Abstract

The effects of boldine [(<I>S</I>)-2, 9-dihydroxyl-1, 10-dimethoxy-aporphine], a major alkaloid in the leaves and bark of Boldo (<I>Peumus boldus</I> Mol.), on neuromuscular transmission were studied using a muscle phrenic-nerve diaphragm preparation. Boldine at concentrations lower than 200 μM preferentially inhibited, after an initial period of twitch augmentation, the nerve-evoked twitches of the mouse diaphragm and left the muscle-evoked twitches unaffected. The twitch inhibition could be restored by neostigmine or washout with Krebs solution. The twitches evoked indirectly and directly were both augmented initially, suggesting that the twitch augmentation induced by boldine was myogenic. Boldine inhibited the acetylcholine-induced contraction of denervated diaphragm dose-dependently with an IC<SUB>50</SUB> value of 13.5 μM. At 50 μM, boldine specifically inhibited the amplitude of the miniature end plate potential. In addition, boldine was similar to <I>d</I>-tubocurarine in its action to reverse the neuromuscular blocking action of α-bungarotoxin. These results showed that the neuromuscular blockade by boldine on isolated mouse phrenic-nerve diaphragm might be due to its direct interaction with the postsynaptic nicotinic acetylcholine receptor.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 76(2), 207-212, 1998-02

    The Japanese Pharmacological Society

References:  24

Codes

  • NII Article ID (NAID)
    10008191630
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    ART
  • ISSN
    00215198
  • NDL Article ID
    4416247
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  NDL  J-STAGE 
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