Lumbar sympathetic nerve responses to somatopressor reflex activation following hindlimb unloading

• Published in: The FASEB journal 2007, Vol.21 (6), p.A882-A882
• Main Authors: Mueller, Patrick J., Friskey, Sarah A., Hasser, Eileen M.
• Format: Article
• Language: English
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fasebj.21.6.A882-b

Exposure to space flight or bedrest results in cardiovascular deconditioning which is associated with increased incidence of orthostatic intolerance. Hindlimb unloaded (HU) rats are a model of cardiovascular deconditioning and exhibit reduced sympatho‐excitation in response to hypotension. It is possible that other forms of sympathoexcitation are also blunted in HU rats. We hypothesized that sympathoexcitatory responses to somatopressor reflex activation were blunted in HU rats. To test this hypothesis rats were maintained under HU or control conditions (CC) for 14 days (n=4 each). Under Inactin anesthesia the central cut end of the sciatic nerve was stimulated while recording mean arterial pressure (MAP) and lumbar sympathetic nerve activity (LSNA). Sciatic stimulation (10–1000 μA, 15 Hz, 1 ms for 10s) produced intensity dependent increases in MAP and LSNA in both groups. Responses in CC and HU rats were similar. For example, at 250 μA, MAP increased 8±2 mmHg in CC and 8±3 mmHg in HU; LSNA increased 65±17% in CC and 64±29% in HU. At 500, μA MAP increased 15±3 mmHg in CC and 13±3 mmHg in HU; LSNA increased 109±33% in CC and 90±32% in HU. These data suggest that unlike baroreceptor unloading, sympathoexcitatory responses to somatopressor reflex activation are unchanged following cardiovascular deconditioning. Furthermore, blunted baroreflex mediated sympathoexcitation does not appear to be due to a generalized reduction in the ability to increase sympathetic outflow following cardiovascular deconditioning. (Supported by HL 55306, AHA 0650161Z).