ATTENUATED BAROREFLEX CONTROL OF SYMPATHETIC-NERVE ACTIVITY AFTER CARDIOVASCULAR DECONDITIONING IN RATS

The effect of cardiovascular deconditioning on baroreflex control of t he sympathetic nervous system was evaluated after 14 days of hindlimb unloading (HU) or the control condition. Rats were chronically instrum ented with catheters and sympathetic nerve recording electrodes for me asurement of mean arterial pressure (MAP) and heart rate (HR) and reco rding of lumbar (LSNA) or renal (RSNA) sympathetic nerve activity. Exp eriments were conducted 24 h after surgery, with the animals in a norm al posture. Baroreflex function was assessed using a logistic function that related HR and LSNA or RSNA to MAP during infusion of phenylephr ine and nitroprusside. Baroreflex influence on HR was not affected by HU. Maximum baroreflex-elicited LSNA was significantly reduced in HU r ats (204 +/- 11.9 vs. 342 +/- 30.6% baseline LSNA), as was maximum ref lex gain (-4.0 +/- 0.6 vs. -7.8 +/- 1.3 %LSNA/mmHg). Maximum barorefle x-elicited RSNA (259 +/- 10.8 vs. 453 +/- 28.0% baseline RSNA), minimu m 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 sig nificantly decreased in KIT rats. Results demonstrate that baroreflex modulation of sympathetic nervous system activity is attenuated after cardiovascular deconditioning in rodents. Data suggest that alteration s in the arterial baroreflex may contribute to orthostatic intolerance after a period of bedrest or spaceflight in humans.