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Clonidine의 아드레날린 수용체에 미치는 영향에 관한 실험적 연구
An Experimental Study on the Adrenergic Mechanism of Clonidine

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Authors
박용재; 이영우; 박찬웅
Issue Date
1982-09
Publisher
서울대학교 의과대학
Citation
Seoul J Med 1982;23(3):299-309
Abstract
Biphasic pressure change and decrease in the heart
rate are well known cardiovascular effects of clonidine.
Extensive pharmacologic studies on the mecha·
nism and site of action of this antihypertensive agent
have been done by many researchers since 1966.
However the results of the studies have been variable.
Clonidine has been reported to lower blood pressure and heart rate in animals and man, by a central action
from the beginning of the study.
It is recently established that in addition to its
central action, clonidine also inhibits the release of
the transmitter from the peripheral sympathetic nerve
endings and that this effect is mediated by presynaptic
inhibitory «-adrenoceptors.
The purpose of this study is to review the cardiovascular
effects of clonidine and to define the relationship
between mechanism of action of clonidine
and adrenoceptors.
The intravenous injection of clonidine (1. 0~50. 0
pg/kg) into rabbits caused bradycardia and biphasic
change in arterial blood pressure, characterized by
an initial transient pressor response followed by a
sustained fall.
The initial pressor response was prolonged and often
potentiated by pretreatment with ganglion blocking
agent, hexamethonium(5mg/kg), but depressor
response and bradycardic effect were not blocked by
it.
The changes of cardiovascular effects of clonidine
after pretreatment with adrenoceptor blocking agents
such as propranolol, phentolamine and yohimbine
were observed.
The pressor effect was blocked by at and a,-receptor
blocker, phentolamine, but not by a,-receptor
blocker, yohimbine or ganglion blocker, hexamethonium.
Hexamethonium inhibited the depressor effect of
clonidine, and additional phentolamine or yohimbine
inhibited it further.
The bradycardic effect was also affected by hexamethonium,
phentolamine and yohimbine respectively.
The results are summerized as follows:
1. The initial pressor effect of clonidine results from
stimulation of a-adrenergic receptors, especially
at-receptors located on peripheral vascular wall.
2. The depressor effect of clonidine involves not only
central inhibition of an adrenergic mechanism but
also peripheral action mediating a-adrenergic receptors
of the a, type.
3. The bradycardic effect of clonidine also results
from activation of both central and peripheral aadrenergic
receptors of the a2 type.
Language
Korean
URI
http://hdl.handle.net/10371/8046
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Medicine (의학과)The Seoul Journal of MedicineThe Seoul Journal of Medicine Vol. 23 No.3 (1982)
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