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Conduction block by clonidine is not mediated by alpha2-adrenergic receptors in rat sciatic nerve fibers.

Authors
 Joong Woo Leem  ;  Yoon Choi  ;  Song Min Han  ;  Mi Ja Yoon  ;  Ji Yeon Sim  ;  Seung Woon Leem 
Citation
 Regional Anesthesia and Pain Medicine, Vol.25(6) : 620-625, 2000 
Journal Title
REGIONAL ANESTHESIA AND PAIN MEDICINE
ISSN
 1098-7339 
Issue Date
2000
MeSH
Adrenergic alpha-Agonists/pharmacology* ; Animals ; Clonidine/pharmacology* ; Male ; Neural Conduction/drug effects* ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, alpha-2/drug effects* ; Receptors, Adrenergic, alpha-2/physiology ; Sciatic Nerve/drug effects* ; Sciatic Nerve/physiology ; Yohimbine/pharmacology
Keywords
Clonidine ; Compound action potential ; Peripheral nerve block ; Adrenergic receptor ; Yohimbine ; Idazoxan
Abstract
BACKGROUND AND OBJECTIVES:
Clonidine, an alpha(2)-adrenergic agonist, has been shown to prolong local anesthesia. It appears that clonidine by itself produces conduction block by acting on peripheral nerves. However, whether clonidine-induced conduction block is mediated through alpha(2)-adrenergic receptors remains unclear. The purpose of this study was to see if clonidine's nerve-blocking action was through alpha(2)-adrenergic receptors by examining clonidine's action in the presence of alpha(2)-adrenergic antagonists.

METHODS:

The compound action potentials (CAPs) evoked by electrical stimuli were recorded from the isolated rat sciatic nerve in a recording chamber. Conduction block was examined by analyzing CAPs with regard to peak amplitude and time-to-peak in the presence of clonidine alone or clonidine plus alpha(2)-adrenergic antagonist yohimbine or idazoxan.

RESULTS:

Both clonidine and yohimbine produced concentration-dependent, reversible, conduction block. Based on concentration-response relationships, the 50% of effective concentration (EC(50)) were estimated to be 1.61 +/- 0.51 mmol/L (mean +/- SD) for clonidine and 51.4 +/- 27.2 micromol/L for yohimbine. A mixture of equal volumes of 2.07 mmol/L clonidine and 55.6 micromol/L yohimbine produced conduction block to a level close to the mean value between conduction blocks induced by 2.07 mmol/L clonidine alone and 55.6 micromol/L yohimbine alone. Addition of idazoxan, a more specific alpha(2)-adrenergic antagonist than yohimbine, to clonidine was without effect on clonidine-induced conduction block.

CONCLUSIONS:

The results indicated that the mixture of clonidine and yohimbine, in which either drug inhibited impulse conduction, produced conduction block in an additive manner, and that clonidine-induced conduction block was not reversed by coapplication with a specific alpha(2)-adrenergic antagonist idazoxan. These data suggest that clonidine's effects likely depend on mechanisms not mediated by alpha(2)-adrenergic receptors.
Full Text
https://www.sciencedirect.com/science/article/pii/S1098733900412277
DOI
10.1053/rapm.2000.16160
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Leem, Joong Woo(임중우) ORCID logo https://orcid.org/0000-0002-1605-2230
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/171854
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