JPET xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kimura, M.
Right arrow Articles by Tsuneki, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kimura, M.
Right arrow Articles by Tsuneki, H.

Noncontractile acetylcholine receptor-operated Ca++ mobilization: suppression of activation by open channel blockers and acceleration of desensitization by closed channel blockers in mouse diaphragm muscle

M Kimura, I Kimura, T Kondoh and H Tsuneki

Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Japan.

The effects of various blockers of the nicotinic acetylcholine receptor- activated ionic channel on noncontractile slow Ca++ mobilization were investigated at the neuromuscular synapse of aequorin-injected diaphragm muscles of mice. Intracellular Ca++ mobilization (Ca++ transients) was evoked in the presence of neostigmine (0.3 microM) by nerve stimulation. Bupivacaine, an open channel blocker, decreased the peak amplitude, whereas chlorpromazine, a closed channel blocker, shortened the duration. Phencyclidine, an open and closed channel blocker, decreased both peak amplitude and duration. beta-Eudesmol, a compound of Atractylodes lancea, clearly and specifically shortened the duration but had little effect on peak amplitude. All the above channel blockers, when given in the same concentration ranges, also blocked the total amount of contractile Ca++ transients. The effects of bupivacaine, chlorpromazine and phencyclidine on noncontractile Ca++ transients were not affected by 5 mM [Ca++]o, whereas the effect of beta-eudesmol was enhanced. Geographutoxin II (0.3 microM), a skeletal muscle Na+ channel blocker, selectively and partly reversibly blocked contractile Ca++ transients without affecting noncontractile ones. These results suggest that: 1) the activation of noncontractile Ca++ mobilization is suppressed by open channel blockers, whereas its desensitization is accelerated by closed channel blockers and 2) activation of the muscle Na+ channel and subsequent release of Ca++ from sarcoplasmic reticulum is not involved in the mechanism of noncontractile Ca++ mobilization. It may reflect the steps of the desensitization process.

Volume 256, Issue 1, pp. 18-23, 01/01/1991
Copyright © 1991 by American Society for Pharmacology and Experimental Therapeutics






Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1991 by the American Society for Pharmacology and Experimental Therapeutics.