. Does nitric oxide buffer arterial blood pressure variability in humans? J Appl Physiol 93: 1466-1470, 2002. First published July 12, 2002 10.1152/ japplphysiol.00287.2002.-Animal studies suggest that nitric oxide (NO) plays an important role in buffering shortterm arterial pressure variability, but data from humans addressing this hypothesis are scarce. We evaluated the effects of NO synthase (NOS) inhibition on arterial blood pressure (BP) variability in eight healthy subjects in the supine position and during 60°head-up tilt (HUT). Systemic NOS was blocked by intravenous infusion of N G -monomethyl-L-arginine (L-NMMA). Electrocardiogram and beat-bybeat BP in the finger (Finapres) were recorded continuously for 6 min, and brachial cuff BP was recorded before and after L-NMMA in each body position. BP and R-R variability and their transfer functions were quantified by power spectral analysis in the low-frequency (LF; 0.05-0.15 Hz) and highfrequency (HF; 0.15-0.35 Hz) ranges. L-NMMA infusion increased supine BP (systolic, 109 Ϯ 4 vs. 122 Ϯ 3 mmHg, P ϭ 0.03; diastolic, 68 Ϯ 2 vs. 78 Ϯ 3 mmHg, P ϭ 0.002), but it did not affect supine R-R interval or BP variability. Before L-NMMA, HUT decreased HF R-R variability (P ϭ 0.03), decreased transfer function gain (LF, 12 Ϯ 2 vs. 5 Ϯ 1 ms/mmHg, P ϭ 0.007; HF, 18 Ϯ 3 vs. 3 Ϯ 1 ms/mmHg, P ϭ 0.002), and increased LF BP variability (P Ͻ 0.0001). After L-NMMA, HUT resulted in similar changes in BP and R-R variability compared with tilt without L-NMMA. Increased supine BP after L-NMMA with no effect on BP variability during HUT suggests that tonic release of NO is important for systemic vascular tone and thus steady-state arterial pressure, but NO does not buffer dynamic BP oscillations in humans. cardiovascular control; head-up tilt; intrinsic rhythmicity LOW-FREQUENCY ARTERIAL PRESSURE oscillations or "Mayer waves" were first described in 1877 (14), yet mechanisms underlying these low-frequency rhythms have remained elusive. Because the magnitude of systolic pressure fluctuations is directly associated with severity of end-organ damage (renal, heart, and brain) and subsequent cardiovascular complications (18), understanding mechanisms of arterial blood pressure oscillations assumes clinical importance.In an effort to explain arterial pressure rhythms occurring at frequencies slower than respiration, at least two hypotheses have been advanced. First, because of intrinsic delays in effector responses to norepinephrine, increases of sympathetic nerve firings are manifested in cardiac and vascular responses with a time delay of ϳ10 s (28). With this construct, waxing and waning of arterial pressures around 0.1 Hz are likely driven by arterial baroreceptor input (9). Second, low-frequency arterial pressure rhythms have been recorded in patients with cervical spinal cord lesions (10) and in isolated mesenteric arteries (21), suggesting the possibility that the peripheral vasculature possesses intrinsic rhythmicity independent of baroreflex feedback loops. The notion that Mayer wa...