Friday, August 23, 2013
Exercise training causes sympathoinhibition through antioxidant effect in the rostral ventrolateral medulla of hypertensive rats
Clin Exp Hypertens. 2012;34(4):278-83.
Kishi T, Hirooka Y, Katsuki M, Ogawa K, Shinohara K, Isegawa K, Sunagawa K.
The authors were interested to know whether exercise training affects sympathetic nerve activity through central mechanisms in stroke-prone spontaneously hypertensive rats (SPSHR). They performed a series of experiments to determine the role of oxidative stress and angiotensin II in this pathway. First, they implanted radio-telemetry system to measure mean arterial pressure and heart rate in both SHRSP and Wistar-Kyoto (WKY) rats. The animals were seperated into 4 groups exercise trained (Treadmill) and non exercise trained for 28 days. After 28 days, urinary norepinephrine was measured as an indicator of sympathetic nerve activity. They measured conscious baroreflex sensitivity by spontaneous sequence method. Thiobarbituric acid-reactive substances were measured from RVLM punches as an indicator of oxidative stress. Tempol, a superoxide dismutase mimetic and angiotensin II were microinjected into the RVLM to determine the pathway. The overall findings are that exercise training in SHRSP caused sympathoinhibition and improved baroreflex sensitivity and reduced oxidative stress through blocked AT1R in the RVLM.
-Madhan
Labels:
AT1R,
Exercise,
Madhan,
oxidative stress,
SHRSP
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