DIFFERENTIAL SYMPATHETIC-NERVE RESPONSES TO NITRIC-OXIDE SYNTHASE INHIBITION IN ANESTHETIZED RATS

Recent studies have suggested that the interaction between the sympath etic nervous system and nitric oxide (NO) or nitrosyl factors may be a n important means by which arterial blood pressure is regulated. We in vestigated whether NO synthase (NOS) inhibition modulates basal sympat hetic nerve discharge (SND) in baroreceptor-innervated and -denervated , chloralose-anesthetized Sprague-Dawley rats. We recorded mean arteri al pressure (MAP), renal SND, and lumbar SND before and after administ ration of the NOS inhibitor, N-G-nitro-L-arginine methyl ester (L-NAME , 20 mg/kg iv). Two minutes after L-NAME administration in barorecepto r-innervated rats, MAP increased (+23 +/- 3 mmHg), whereas renal (-45 +/- 6%, n = 7) and lumbar (-35 +/- 2%, n = 6) SND significantly decrea sed from control levels. These changes persisted for up to 20 min afte r L-NAME administration. In baroreceptor-denervated rats, L-NAME incre ased MAP (+40 +/- 6 mmHg) and decreased lumbar SND (n = 7) (-37 +/- 10 % from control at 20 min post-L-NAME). In contrast, renal SND progress ively increased (+33 +/- 8% at 20 min post-L-NAME) from control after L-NAME administration in baroreceptor-denervated rats (n = 7). These r esults demonstrate that NOS inhibition can produce nonuniform changes in SND in baroreceptor-denervated rats and suggest that endogenous nit rosyl factors provide tonic excitation to lumbar SND, whereas they pro vide a tonic restraint to renal SND.