RELATIONSHIP BETWEEN SYMPATHETIC NERVOUS-SYSTEM ACTIVITY, BAROREFLEX AND CARDIOVASCULAR EFFECTS AFTER ACUTE NITRIC-OXIDE SYNTHESIS INHIBITION IN HUMANS

Objective: To examine the cardiovascular effects of acute systemic nit ric oxide synthesis inhibition in humans in relation to the possible i nvolvement of changes in sympathetic nervous system activity or in the baroreceptor reflex. Design: Placebo or N-G-monomethyl-L-arginine (25 0 mg by intravenous infusion for 5 min) was administered to seven heal thy male volunteers according to a random, double-blind sequence. Meth ods: Blood pressure and heart rate were measured non-invasively using a Finapres device from 20 min before to 80 min after starting infusion ; beat-to-beat variability of blood pressure, pulse interval and systo lic blood pressure and pulse interval covariation were assessed by mea ns of spectral and sequence analysis methods. Under basal conditions a nd 15 min and 60 min after infusion, we measured stroke volume and ind ices of cardiac systolic and diastolic function by echocardiography, f orearm blood flow by strain-gauge venous occlusion plethysmography, an d plasma catecholamine levels. Results: Compared with placebo, adminis tration of N-G-monomethyl-L arginine caused a transient increase in bl ood pressure and reduction in heart rate. Stroke volume and indices of cardiac function did not change significantly, whereas cardiac index and forearm blood flow were significantly reduced after 15 min. Spectr al analysis of blood pressure and pulse interval showed a significant reduction of power spectral density in the low frequencies (0.03-0.15 Hz) that persisted 60 min after infusion. The plasma noradrenaline lev el was significantly reduced after 15 min. No change in baroreflex eng agement or sensitivity was detected by the cross-spectral or the seque nce method. Conclusions: Acute systemic nitric oxide synthesis inhibit ion transiently increases blood pressure and reduces heart rate and ca rdiac index. The acute hypertensive response to N-G-monomethyl-L-argin ine is dependent neither on sympathetic nervous system activity, which is probably reduced as a consequence of baroreceptor reflex activatio n, nor on baroreceptor reflex sensitivity, which is not impaired.