INHIBITION OF NO SYNTHESIS DOES NOT POTENTIATE DYNAMIC CARDIOVASCULAR-RESPONSE TO SYMPATHETIC-NERVE ACTIVITY

We examined whether the inhibition of nitric oxide (NO) synthesis pote ntiates the dynamic sympathetic regulation of the cardiovascular syste m through the baroreflex. In anesthetized rabbits, me imposed random p ressure perturbations on the isolated carotid sinuses to evoke random changes in sympathetic nerve activity (SNA). We estimated the transfer functions from SNA to both aortic pressure (AoP) and heart rate (HR). The inhibition of NO synthesis by N-G-monomethyl-L-arginine (L-NMMA, 40 mg/kg) altered neither the transfer function from SNA to AoP nor th at from SNA to HR. In contrast, sodium nitroprusside (3-6 mu g.kg(-1). min(-1)) significantly decreased the steady-state gain (40.3 +/- 11.7% , of the control, P < 0.05) of the transfer function from SNA to AoP w ithout affecting the HR responses. We conclude that the basal release of NO may have a role in the tonic blood pressure regulation, whereas it may not be involved in the dynamic sympathetic regulation of AoP or NR through the baroreflex.