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Medial prefrontal cortex acetylcholine injection-induced hypotension: the role of hindlimb vasodilationThe 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.
Document ID
20040141661
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Crippa, G. E.
(School of Medicine of Ribeirao Preto-USP 14049-900, Ribeirao Preto, Brazil)
Lewis, S. J.
Johnson, A. K.
Correa, F. M.
Date Acquired
August 22, 2013
Publication Date
February 14, 2000
Publication Information
Publication: Journal of the autonomic nervous system
Volume: 79
Issue: 1
ISSN: 0165-1838
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: HL57472
CONTRACT_GRANT: HL14388
Distribution Limits
Public
Copyright
Other
Keywords
Non-NASA Center
NASA Discipline Regulatory Physiology
NASA Program Biomedical Research and Countermeasures

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