The present study evaluated the possible changes in the autonomic control of heart rate in the hypertensive model induced by the inhibition of nitric oxide synthase. Rats were treated with N(G)-nitro-L-arginine methyl ester (L-NAME group) in the drinking water during 7 days, whereas control groups were treated with tap water (control group) or with the N(G)-nitro-D-arginine methyl ester (D-NAME group), an inactive isomer of the L-NAME molecule. The L-NAME group developed hypertension and tachycardia. The sequential blockade of the autonomic influences with propranolol and methylatropine indicated that the intrinsic heart rate did not differ among groups and revealed a sympathetic overactivity in the control of heart rate in the L-NAME group. The spectral density power of heart rate, calculated using fast-Fourier transformation, indicated a reduced variability in the low-frequency band (0.20-0.60 Hz) for the L-NAME group. The baroreflex sensitivity was also attenuated in these animals when compared with the normotensive control or D-NAME group. Overall, these data indicate cardiac sympathetic overactivity associated with a decreased baroreflex sensitivity in L-NAME hypertensive rats.

The goal of this study was to determine the baroreflex influence on systolic arterial pressure (SAP) and pulse interval (PI) variability in conscious mice. SAP and PI were measured in C57Bl/6J mice subjected to sinoaortic deafferentation (SAD, n = 21) or sham surgery (n = 20). Average SAP and PI did not differ in SAD or control mice. In contrast, SAP variance was enhanced (21 +/- 4 vs. 9.5 +/- 1 mmHg2) and PI variance reduced (8.8 +/- 2 vs. 26 +/- 6 ms2) in SAD vs. control mice. High-frequency (HF: 1-5 Hz) SAP variability quantified by spectral analysis was greater in SAD (8.5 +/- 2.0 mmHg2) compared with control (2.5 +/- 0.2 mmHg2) mice, whereas low-frequency (LF: 0.1-1 Hz) SAP variability did not differ between the groups. Conversely, LF PI variability was markedly reduced in SAD mice (0.5 +/- 0.1 vs. 10.8 +/- 3.4 ms2). LF oscillations in SAP and PI were coherent in control mice (coherence = 0.68 +/- 0.05), with changes in SAP leading changes in PI (phase = -1.41 +/- 0.06 radians), but were not coherent in SAD mice (coherence = 0.08 +/- 0.03). Blockade of parasympathetic drive with atropine decreased average PI, PI variance, and LF and HF PI variability in control (n = 10) but had no effect in SAD (n = 6) mice. In control mice, blockade of sympathetic cardiac receptors with propranolol increased average PI and decreased PI variance and LF PI variability (n = 6). In SAD mice, propranolol increased average PI (n = 6). In conclusion, baroreflex modulation of PI contributes to LF, but not HF PI variability, and is mediated by both sympathetic and parasympathetic drives in conscious mice.

The HIV group presented in baseline conditions, a shift of cardiac sympathovagal balance, an exacerbated response of the LF component during the tilt test, and an ineffective cardiac vagal response to the cold-face test suggesting sympathetic and parasympathetic dysfunction. AIDS patients receiving HAART did not present these autonomic alterations.

Heart rate variability (HRV) is a psychophysiological phenomenon with broad implications, providing an accessible index of vagal function, underpinning psychological constructs, including the capacity for social engagement and emotion regulation, and may predict future morbidity and mortality. However, the lack of reference values for short-term HRV indices for participants of both sexes across the age spectrum is a limiting factor. This was the objective of the present study. Resting electrocardiographic records were obtained from 13,214 participants (both sexes, 35-74 years), and HRV indices in time and frequency domains (mean ± SD) were determined from 5-min records. Results were based on a subsample of 2,874 nonmedicated, healthy participants stratified by sex across 10-year age groupings. Men showed lower heart rate (HR, 64 ± 8 bpm vs. 68 ± 8 bpm, p < .05) and normalized high frequency (HF; 39.4 ± 18.0 normalized units [n.u.] vs. 50.4 ± 18.5 n.u., p < .05) than women, and higher N-N variance (2,214 ± 1,890 ms vs. 1,883 ± 1,635 ms , p < .05), standard deviation of all N-N intervals (SDNN; 43.7 ± 17.3 ms vs. 40.3 ± 15.8 ms, p < .05) and LF/HF (2.30 ± 2.68 vs. 1.33 ± 1.82, p < .05). HR and HF (n.u.) were also higher in younger than older women. LF/HF was lower in women than men. Percentile curves showed almost all HRV indices decreasing with aging. The availability of short-term, resting-state HRV reference values in a large sample of healthy and nonmedicated participants from 35-74 years will provide a valuable tool for researchers, clinicians, and those in the quantified-self community.

Abstract-The sympathetic outflow appears to be capable of displaying a rhythmicity synchronous with cardiovascular Mayer's waves even after spinal section. To test the hypothesis that spinal sympathetic low frequency (LF) oscillation can be enhanced during sympathetic excitation, we recorded cardiac sympathetic nerve activity (SNA), R-R interval, arterial pressure, and ventilation in 9 unanesthetized decerebrate-vagotomized cats before and after C1 spinal section. LF and high frequency (HF) components were detected in the variability of SNA, R-R interval, and systolic arterial pressure both before and after spinal section. In this latter condition, a significant coherence between LF SNA and LF R-R was present in 5 animals, whereas HF SNA and HF R-R were correlated in 4 animals. During an excitatory sympathetic spinal reflex elicited by aortic constriction, the efferent sympathetic firing was markedly enhanced (from 7Ϯ2 to 33Ϯ7 spikes/s); concomitantly, the powers of both LF SNA and HF SNA were also increased. Coherence between LF SNA and LF R-R became significant in all cases, whereas HF SNA and HF R-R became correlated in 6 animals. In 3 animals, the reflex sympathetic excitation was no longer elicitable after interrupting a vast contingent of sympathetic afferents by means of thoracic dorsal root section. We report for the first time that LF and HF oscillations are detectable in SNA, R-R interval, and systolic arterial pressure variabilities of decerebrate-vagotomized spinal cats and that an excitatory spinal reflex is capable of increasing the power of both SNA spectral components. (Hypertension. 2000;36:1029-1034.)