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Department of Veterinary Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211
Attenuated baroreflex-mediated increases
in renal sympathetic nerve activity (RSNA) in hindlimb unloaded (HU)
rats apparently are due to changes within the central nervous system.
We hypothesized that GABAA receptor-mediated inhibition of
the rostral ventrolateral medulla (RVLM) is increased after hindlimb
unloading. Responses to bilateral microinjection of the
GABAA antagonist (
)-bicuculline methiodide (BIC) into the
RVLM were examined before and during caudal ventrolateral medulla
(CVLM) inhibition in Inactin-anesthetized control and HU rats.
Increases in mean arterial pressure (MAP), heart rate (HR), and RSNA in
response to BIC in the RVLM were significantly enhanced in HU rats.
Responses to bilateral CVLM blockade were not different. When remaining
GABAA inhibition in the RVLM was blocked by BIC during CVLM
inhibition, the additional increases in MAP and RSNA were significantly
greater in HU rats. These data indicate that GABAA
receptor-mediated inhibition of RVLM neurons is augmented after
hindlimb unloading. Effects of input from the CVLM were unaltered.
Thus, after cardiovascular deconditioning in rodents, the attenuated
increase in sympathetic nerve activity in response to hypotension is
associated with greater GABAA receptor-mediated inhibition
of RVLM neurons originating at least in part from sources other than
the CVLM.
microgravity; cardiovascular deconditioning; sympathetic nervous system; bedrest; orthostatic intolerance; spaceflight; caudal ventrolateral medulla
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