RT Journal Article
SR Electronic
T1 Enhancing effect by nicotinic acetylcholine receptor channel blockers, including beta-eudesmol, on succinylcholine-induced inhibition of twitch tension and intracellular Ca++ in mouse diaphragm muscle.
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 24
OP 28
VO 256
IS 1
A1 I Kimura
A1 H Tsuneki
A1 T Kondoh
A1 M Kimura
YR 1991
UL http://jpet.aspetjournals.org/content/256/1/24.abstract
AB To elucidate the mechanism of neuromuscular block by succinylcholine, nerve-evoked changes in intracellular Ca(++)-aequorin luminescence and twitch tension were measured simultaneously in the presence of several different types of blockers for the nicotinic acetylcholine receptor channel. Mouse diaphragm muscles were pretreated for 30 to 60 min with 3 to 40 microM bupivacaine, chlorpromazine, phencyclidine and beta-eudesmol. The effects of these noncompetitive blockers on the succinylcholine-induced response were also compared with those for pancuronium. These channel blockers potentiated (2- to 10-fold) both the blocking effects on intracellular Ca++ and twitch tension of succinylcholine (13-100 microM), but not the pancuronium (0.3-1.1 microM)-induced block. These channel blockers also suppressed succinylcholine (1.3-5 microM)-induced enhancement of evoked Ca++ transients. On the other hand, the channel blockers inhibited the succinylcholine (2.5-100 microM)-induced increase in basal Ca++ transients. These results suggest that neuromuscular block induced by succinylcholine is mainly due to desensitization of the nicotinic acetylcholine receptor.