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Departments of Veterinary Biomedical Sciences and Physiology, Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211
The effect of cardiovascular
deconditioning on baroreflex control of the sympathetic nervous system
was evaluated after 14 days of hindlimb unloading (HU) or the control
condition. Rats were chronically instrumented with catheters and
sympathetic nerve recording electrodes for measurement of mean arterial
pressure (MAP) and heart rate (HR) and recording of lumbar (LSNA) or
renal (RSNA) sympathetic nerve activity. Experiments were conducted 24 h after surgery, with the animals in a normal posture. Baroreflex function was assessed using a logistic function that related HR and
LSNA or RSNA to MAP during infusion of phenylephrine and nitroprusside. Baroreflex influence on HR was not affected by HU. Maximum
baroreflex-elicited LSNA was significantly reduced in HU rats (204 ± 11.9 vs. 342 ± 30.6% baseline LSNA), as was maximum reflex
gain (
4.0 ± 0.6 vs.
7.8 ± 1.3 %LSNA/mmHg).
Maximum baroreflex-elicited RSNA (259 ± 10.8 vs. 453 ± 28.0%
baseline RSNA), minimum baroreflex-elicited RSNA (
2 ± 2.8 vs. 13 ± 4.5% baseline RSNA), and maximum gain (
5.8 ± 0.5 vs.
13.6 ± 3.1 %RSNA/mmHg) were significantly decreased in HU rats. Results demonstrate that baroreflex modulation of sympathetic nervous system activity is attenuated after cardiovascular deconditioning in rodents. Data suggest that alterations in the arterial baroreflex may contribute to orthostatic intolerance after a
period of bedrest or spaceflight in humans.
microgravity; hindlimb unweighting; blood pressure; bedrest; orthostatic intolerance
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