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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by DEGUCHI, T.
Right arrow Articles by NARAHASHI, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by DEGUCHI, T.
Right arrow Articles by NARAHASHI, T.
Journal of Pharmacology And Experimental Therapeutics, Vol. 176, Issue 2, 423-433, 1971
Copyright © 1971 by American Society for Pharmacology and Experimental Therapeutics


EFFECTS OF PROCAINE ON IONIC CONDUCTANCES OF END-PLATE MEMBRANES

TAKEHIKO DEGUCHI 1 and TOSHIO NARAHASHI 1

1 Department of Physiology and Pharmacology, Duke University Medical Center, Durham, North Carolina

The ionic mechanisms underlying the prolongation of the end-plate potential caused by application of procaine have been studied by means of voltage clamp techniques with the sartorius muscle fibers of the frog. The end-plate currents were recorded when the membrane was clamped at various potential levels in the muscle treated with glycerol to avoid contraction. Before application of procaine, the sodium component of the end-plate current measured at the equilibrium potential for potassium (-100 mV) was larger in peak amplitude and slower in decay than the potassium component measured at the equilibrium potential for sodium (+50 mV). The end-plate conductance was constant at the membrane potentials ranging from +50 to -100 mV but decreased slightly at inside more negative membrane potentials. The equilibrium potential for the end-plate current was estimated to be -4.2 mV on an average. Procaine (3.6 x 10-5 sim 3.6 x 10-4 M) suppressed the peak amplitudes of both sodium and potassium components of the end-plate current, the sodium current being slightly more affected than the potassium current. The equilibrium potential for the end-plate current was not significantly affected by procaine. The time course of the sodium current underwent marked changes by treatment with procaine; the time to peak was shortened, and the initial falling phase was accelerated and was followed by a very slow terminal phase. The current-voltage relation for the terminal current was different from that for the peak current. The time to peak potassium current was not affected by procaine, but the falling phase was slowed. The dose-response relations for the time parameters of the end-plate current are different from those for the peak amplitude, suggesting that different mechanisms are involved. The possibility of separate sodium and potassium ionic channels in the end-plate membrane is discussed.

Submitted on December 3, 1969
Accepted on October 2, 1970




This article has been cited by other articles:


Home page
ScienceHome page
E. Albuquerque, A. Eldefrawi, M. Eldefrawi, N. Mansour, and M. Tsai
Amantadine: neuromuscular blockade by suppression of ionic conductance of the acetylcholine receptor
Science, February 17, 1978; 199(4330): 788 - 790.
[Abstract] [PDF]


Home page
ScienceHome page
K. Kuba, E. X. Albuquerque, and E. A. Barnard
Diisopropylfluorophosphate: Suppression of Ionic Conductance of the Cholinergic Receptor
Science, August 31, 1973; 181(4102): 853 - 856.
[Abstract] [PDF]




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

Copyright © 1971 by the American Society for Pharmacology and Experimental Therapeutics.