Medial prefrontal cortex acetylcholine injection-induced hypotension:: the role of hindlimb vasodilation

被引:21
作者
Crippa, GE
Lewis, SJ
Johnson, AK
Corrêa, FMA [1 ]
机构
[1] USP, Sch Med, Dept Pharmacol, BR-14049900 Ribeirao Preto, Brazil
[2] Univ Iowa, Dept Pharmacol, Iowa City, IA 52242 USA
[3] Univ Iowa, Ctr Cardiovasc, Iowa City, IA 52242 USA
[4] Univ Iowa, Dept Psychol, Iowa City, IA 52242 USA
来源
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM | 2000年 / 79卷 / 01期
关键词
rat; blood pressure; hypotension; brain; cingulate cortex; medial prefrontal cortex; neurogenic vasodilation; acetylcholine;
D O I
10.1016/S0165-1838(99)00091-0
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The injection of acetylcholine (ACh) into the cingulate region of the medial prefrontal cortex (MPFC) causes a marked fall in arterial blood pressure which is not accompanied by changes in heart rate. The purpose of the present study was to investigate the hemodynamic basis for this stimulus-induced hypotension in Sprague-Dawley rats. The study was designed to determine whether a change in the vascular resistance of hindlimb, renal or mesenteric vascular beds contributes to the fall in arterial pressure in response to ACh injection into the cingulate cortex. Miniature pulsed-Doppler flow probes were used to measure changes in regional blood flow and vascular resistance. The results indicated that the hypotensive response was largely due to a consistent and marked vasodilation in the hindlimb vascular bed. On this basis, an additional experiment was then undertaken to determine the mechanisms that contribute to hindlimb vasodilation. The effect of interrupting the autonomic innervation of one leg on the hindlimb vasodilator response was tested. Unilateral transection of the lumbar sympathetic chain attenuated the cingulate ACh-induced vasodilation in the ipsilateral, but not in the contralateral hindlimb. These results suggest that the hypotensive response to cingulate cortex-ACh injection is caused by skeletal muscle vasodilation mediated by a sympathetic chain-related vasodilator system. (C) 2000 Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:1 / 7
页数:7
相关论文
共 25 条
[1]   Depression of endothelial nitric oxide synthase but increased expression of endothelin-1 immunoreactivity in rat thoracic aortic endothelium associated with long-term, but not short-term, sympathectomy [J].
Aliev, G ;
Ralevic, V ;
Burnstock, G .
CIRCULATION RESEARCH, 1996, 79 (02) :317-323
[2]   ELECTROPHYSIOLOGICAL ANALYSIS OF NEUROGENIC VASODILATATION IN THE ISOLATED LINGUAL ARTERY OF THE RABBIT [J].
BRAYDEN, JE ;
LARGE, WA .
BRITISH JOURNAL OF PHARMACOLOGY, 1986, 89 (01) :163-171
[3]   NEUROGENIC MUSCARINIC VASODILATION IN THE CAT - AN EXAMPLE OF ENDOTHELIAL CELL-INDEPENDENT CHOLINERGIC RELAXATION [J].
BRAYDEN, JE ;
BEVAN, JA .
CIRCULATION RESEARCH, 1985, 56 (02) :205-211
[4]   THE INVOLVEMENT OF THE ANTERIOR CINGULATE CORTEX IN BLOOD-PRESSURE CONTROL [J].
BURNS, SM ;
WYSS, JM .
BRAIN RESEARCH, 1985, 340 (01) :71-77
[5]   Cardiovascular response to the injection of acetylcholine into the anterior cingulate region of the medial prefrontal cortex of unanesthetized rats [J].
Crippa, GE ;
Peres-Polon, VL ;
Kuboyama, RH ;
Corrêa, FMA .
CEREBRAL CORTEX, 1999, 9 (04) :362-365
[6]   Use-dependent loss of active sympathetic neurogenic vasodilation after nitric oxide synthase inhibition in conscious rats - Evidence for the presence of preformed stores of nitric oxide-containing factors [J].
Davisson, RL ;
Shaffer, RA ;
Johnson, AK ;
Lewis, SJ .
HYPERTENSION, 1996, 28 (03) :347-353
[7]   Neurogenically derived nitrosyl factors mediate sympathetic vasodilation in the hindlimb of the rat [J].
Davisson, RL ;
Possas, OS ;
Murphy, SP ;
Lewis, SJ .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1997, 272 (05) :H2369-H2376
[8]  
DELGADO JOSE M R., 1960, PHYSIOL REVS, V40, P146
[10]   Pressor and depressor sites are intermingled in the cingulate cortex of the rat [J].
Fisk, GD ;
Wyss, JM .
BRAIN RESEARCH, 1997, 754 (1-2) :204-212