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We have reported that baroreflex bradycardia evoked by stimulating the aortic nerve is blunted at the onset of voluntary static exercise in conscious cats and spontaneous exercise in decerebrate cats, suggesting that central command may inhibit the arterial baroreceptors-heart rate reflex (Komine et al. 2003; Murata et al. 2004; Matsukawa et al. 2006, 2007). Although the interaction between central command and arterial baroreflex should occur within the lower brainstem, an underlying neural mechanism remained unknown. We hypothesized that endogenous release of nitric oxide in the brain played a role in inhibiting the cardiac component of arterial baroreflex at the onset of exercise. To test the hypothesis, we examined the effect of intracisternal injection of a nitric oxide synthesis inhibitor (L-NAME) on the blunted baroreflex bradycardia at the onset of spontaneous exercise in decerebrate cats. Arterial blood pressure (AP) was rapidly elevated by occluding the abdominal aorta above the level of the kidneys. The baroreflex bradycardia evoked by an increase in AP due to the occlusion was blunted at the onset of spontaneous active exercise and fictive exercise with muscle paralysis. The inhibition of baroreflex bradycardia at the onset of spontaneous exercise was attenuated by intracisternal injection of L-NAME, but not by D-NAME. Thus central command may cause an endogenous release of nitric oxide in the lower brainstem, which has a role in inhibiting the cardiac component of the arterial baroreflex. [J Physiol Sci. 2008;58 Suppl:S48]
