OBJECTIVETo investigate the effects of central oxidative stress on the baroreflex function and central mechanism responsible for the attenuated baroreflex sensitivity (BRS) in spontaneously hypertensive rats (SHR).

METHODSMale 24-week-old SHR and normal rats were anesthetized with urethane and alpha-chloralose. Intravenous injection of phenylephrine (PE) and sodium nitroprusside (NP) evoked arterial baroreflex. The ratio of change in heart rate (HR) to change in mean aortic pressure (MAP) represented the baroreflex sensitivity (BRS). Alteration in BRS was evaluated before and after intracerebroventricular administration of superoxide dismutase (SOD) mimetic tempol or SOD inhibitor diethyldithiocarbamic acid (DETC).

RESULTSBRS in hypertensive rats was significantly lower than that in normal rats (PE: P < 0.01, NP: P < 0.01). Intracerebroventricular administration of Tempol significantly improved BRS in hypertensive rats (P < 0.05), but not in normal rats. In contrast, DETC decreased BRS to a greater extent in normal group than in hypertension group (P < 0.05). MDA content in hypothalamus of hypertensive rats was higher than that of normal rats (P < 0.01), whereas total antioxidant capacity, total SOD, CuZn-SOD, catalase activity were lower in hypertensive rats than in normal rats (P < 0.05).

CONCLUSIONAttenuated baroreflex function in hypertensive rats is associated with central oxidative stress, which is linked to decreases in antioxidant enzyme activity and antioxidative capacity in the brain.