Nicardipine inhibits axon conduction but causes dual changes of acetylcholine release in the mouse motor nerve

C. C. Chang, L. C. Chiou, L. L. Hwang, S. J. Hong, C. Y. Huang

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

The effects of nicardipine, a dihydropyridine Ca2+-channel antagonist, on neuromuscular transmission and impulse-evoked release of acetylcholine were compared with those of nifedipine. In the isolated mouse phrenic nerve diaphragm, nicardipine (50 μM), but not nifedipine (100 μM), induced neuromuscular block, fade of tetanic contraction, and dropout or all-or-none block of end-plate potentials. Nicardipine had no significant effect on the resting membrane potential and the amplitude of miniature end-plate potentials but increased the frequency and caused the appearance of large size miniature potentials. The quantal contents of evoked end-plate potentials were increased. In the presence of tubocurarine, however, nicardipine depressed the amplitude of end-plate potentials. The compound nerve action potential was also decreased. It is concluded that nicardipine blocks neuromuscular transmission by acting on Na+ channels and inhibits axonal conduction. Nicardipine appeared to affect the evoked release of acetylcholine by dual mechanisms, i.e., an enhancement presumably by an agonist action on Ca2+ channels, like Bay K 8644 and nifedipine, and inhibition by an effect on Na+ channels, like verapamil and diltiazem. In contrast with its inactivity on the amplitude of miniature end-plate potentials, depolarization of the end plate in response to succinylcholine was greatly depressed. The contractile response of baby chick biventer cervicis muscle to exogenous acetylcholine was noncompetitively antagonized by nicardipine (10 μM), but was unaffected by nifedipine (30 μM). These results may implicate that nicardipine blocks the postsynaptic acetylcholine receptor channel by enhancing receptor desensitization or by a use-dependent effect.

Original languageEnglish
Pages (from-to)1493-1498
Number of pages6
JournalCanadian Journal of Physiology and Pharmacology
Volume67
Issue number12
Publication statusPublished - 1989
Externally publishedYes

Fingerprint

Nicardipine
Acetylcholine
Axons
Nifedipine
Excitatory Postsynaptic Potentials
Miniature Postsynaptic Potentials
Neuromuscular Blockade
Electrophysiological Refractory Period
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
Tubocurarine
Phrenic Nerve
Succinylcholine
Diltiazem
Cholinergic Receptors
Verapamil
Diaphragm
Membrane Potentials
Action Potentials
Muscles

Keywords

  • Acetylcholine receptor desensitization
  • Acetylcholine release
  • Calcium channel antagonists
  • Neuromuscular transmission
  • Nicardipine

ASJC Scopus subject areas

  • Physiology
  • Pharmacology

Cite this

Nicardipine inhibits axon conduction but causes dual changes of acetylcholine release in the mouse motor nerve. / Chang, C. C.; Chiou, L. C.; Hwang, L. L.; Hong, S. J.; Huang, C. Y.

In: Canadian Journal of Physiology and Pharmacology, Vol. 67, No. 12, 1989, p. 1493-1498.

Research output: Contribution to journalArticle

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