Abstract
We recently demonstrated that the baroreflex bradycardia evoked by stimulation of the aortic depressor nerve (ADN) is attenuated immediately before or at the onset of voluntary static exercise in conscious cats, whereas the ADN stimulation-induced depressor response remains the same (Komine et al. Am J Physiol, H516-526, 2003). This result suggested that central command blunts the cardiac component, but not vasomotor component, of the aortic baroreflex at the onset of voluntary static exercise. The aim of the present study was to examine whether nitric oxide (NO) contributes to the inhibition of the cardiac component of the aortic baroreflex by central command, by administering a synthesis inhibitor of NO (L-NAME, 5mg/kg i.v.) using conscious cats. When the ADN was stimulated at rest, heart rate decreased by 36±6 beats/min and arterial blood pressure reduced by 10±2 mmHg. The ADN stimulation-induced bradycardia was attenuated at the onset of exercise to 63±8% of the preexercise bradycardia. Following L-NAME, the reduction of the baroreflex bradycardia seen at the onset of exercise was absent. This finding suggested that L-NAME blunted the attenuating effect of central command on the ADN stimulation-induced bradycardia. Therefore it is likely that endogenous nitric oxide released in the brain plays a role in the inhibition of the cardiac component of the aortic baroreflex by central command at the onset of voluntary static exercise. [Jpn J Physiol 54 Suppl:S95 (2004)]
