INHIBITION OF BASAL AND REFLEX-MEDIATED SYMPATHETIC ACTIVITY IN THE RVLM BY NITRIC-OXIDE

We examined possible functional roles for nitric oxide (NO) in the ros tral ventrolateral medulla (RVLM), which is the final area for integra tion of sympathetic nerve activity (SNA) within the brain stem. Chlora lose-anesthetized cats were completely baro- and chemoreceptor denerva ted, the RVLM was exposed for microinjections, and preganglionic SNA w as recorded from the white ramus of the 3rd thoracic segment. Injectio ns of N-G-nitro-L-arginine (L-NNA), an inhibitor of NO synthase, but n ot of N-G-nitro-D-arginine, caused distinct increases in SNA and arter ial blood pressure (BP). Excitatory somatosympathetic reflex amplitude s evoked by electrical stimulation of the 4th intercostal nerve were s ignificantly increased by L-NNA whereas inhibitory responses to barore flex activation by stimulation of the carotid sinus nerve were not aff ected. The effects of L-NNA were counteracted by the NO-donor compound s glyceryltrinitrate and S-nitroso-N-acetylpenicillamine, which decrea sed BP and SNA below control values at higher doses. These results sug gest that endogenous NO, in addition to its peripheral actions, modula tes the central nervous control of cardiovascular functions by reducti on of basal sympathetic tone and by attenuation of excitatory reflex r esponses.