AJP - Heart Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 274: H1194-H1201, 1998;
0363-6135/98 $5.00
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Taylor, J. A.
Right arrow Articles by Davy, K. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Taylor, J. A.
Right arrow Articles by Davy, K. P.
Vol. 274, Issue 4, H1194-H1201, April 1998

Low-frequency arterial pressure fluctuations do not reflect sympathetic outflow: gender and age differences

J. Andrew Taylor1, Todd D. Williams1, Douglas R. Seals2, and Kevin P. Davy2

1 Hebrew Rehabilitation Center for Aged, Beth Israel Deaconess Medical Center, and Harvard Medical School Division on Aging, Boston, Massachusetts 02167; 2 Department of Kinesiology, University of Colorado, Boulder 80309; and Department of Medicine (Cardiology and Geriatric Medicine), University of Colorado Health Sciences Center, Denver, Colorado 80262

    ABSTRACT
Top
Abstract
Introduction
Methods
Results
Discussion
References

Low-frequency arterial pressure oscillations (Mayer waves) have been proposed as an index of vascular sympathetic outflow. However, cross-sectional differences in these pressure oscillations may not reflect different levels of sympathetic nervous outflow in humans. Three groups of healthy subjects with characteristically different sympathetic nervous outflow were studied: young females (n = 10, 18-28 yr), young males (n = 11, 18-29 yr), and older males (n = 13, 60-72 yr). Average R-R interval, arterial pressures, and systolic pressure variability at the Mayer wave frequency (0.05-0.15 Hz) did not differ among the three groups. Diastolic pressure Mayer wave variability was similar in young females vs. young males (39 ± 10 vs. 34 ± 5 mmHg2) and lower in older males vs. young males (14 ± 2 mmHg2; P < 0.05). In contrast, muscle sympathetic activity was lowest in young females (892 ± 249 total activity/min) and highest in older males (3,616 ± 528 total activity/min; both P < 0.05 vs. young males: 2,505 ± 285 total activity/min). Across the three groups, arterial pressure Mayer wave variability did not correlate with any index of sympathetic activity. Our results demonstrate that arterial pressure Mayer wave amplitude is not a surrogate measure of vascular sympathetic outflow.

autonomic nervous system; power spectral analysis; heart rate variability

    INTRODUCTION
Top
Abstract
Introduction
Methods
Results
Discussion
References

THE ORIGINAL OBSERVATIONS of arterial pressure waves at a frequency lower than the respiratory rate indicated that this oscillation may arise from an inherent rhythmicity in cardiovascular vasomotor centers (11, 14, 28). Subsequent research refined this hypothesis, demonstrating that 10-s arterial pressure Mayer waves can be produced by a central (37) or baroreceptor (15)-mediated sympathetic oscillation coupled with a delay in the alpha -adrenergic vasoconstrictor response (25). Although most postulated mechanisms necessitate a vascular sympathetic effector for Mayer wave generation, they do not require proportionality between vascular sympathetic tone and Mayer wave amplitude. Despite this, differences or alterations in low-frequency arterial pressure variability under conditions that prominently change autonomic tone in humans have been presumed to represent proportional changes in vascular sympathetic outflow (12, 24, 27, 38), although the proportionality between low-frequency arterial pressure variability and directly measured sympathetic nervous activity is unclear (33). Findings in animals suggest that Mayer wave amplitude is not proportional to the level of mean sympathetic nervous outflow (46) but that it is related to the level of sympathetic oscillations (36).

We hypothesized that mean sympathetic activity and Mayer wave amplitude are not correlated but that the levels of Mayer wave frequency oscillations in arterial pressure and sympathetic activity are correlated. To elucidate whether cross-sectional differences in Mayer wave amplitude represent any aspect of vascular sympathetic activity, we assessed sympathetic activity and Mayer wave amplitude in three groups of healthy subjects with characteristically different levels of muscle sympathetic outflow. Young females exhibit less basal sympathetic nerve activity than young males, who in turn exhibit less basal sympathetic nerve activity than older males (30). Frequency domain analysis of arterial pressures and directly measured muscle sympathetic nerve activity afforded insight to Mayer wave amplitude and its relation to average sympathetic nervous outflow and to sympathetic nervous oscillations. Our results suggest that cross-sectional differences in Mayer wave amplitude do not provide insight to differences in vascular sympathetic outflow.

    METHODS
Top
Abstract
Introduction
Methods
Results
Discussion
References

Subjects. We assessed data from 10 young females [aged 18-28 yr; mean, 22 ± 4 (SE) yr], 11 young males [18-29 yr; mean, 24 ± 4 (SE) yr], and 13 older males [60-72 yr; mean, 65 ± 4 (SE) yr]. Subjects were not on medication, were not obese (body mass index range 17.9-28.7 for all subjects), and were not smokers. All older subjects were free of any signs or symptoms of overt coronary heart disease based on medical history and resting and maximal exercise electrocardiograms. The study protocol was approved by the Institutional Review Boards of the University of Colorado and the Hebrew Rehabilitation Center for Aged. All subjects gave verbal and written informed consent.

Protocol and measurements. Lead II of the electrocardiogram, beat-to-beat arterial pressures, respiratory excursions, and muscle sympathetic nerve activity were recorded continuously during 5 min of controlled frequency breathing (15 breaths/min, 0.25 Hz) with subjects in the supine position. Figure 1 shows representative tracings from a young female, young male, and older male.


View larger version (53K):
[in this window]
[in a new window]
  		Fig. 1.   Raw data from a representative young female, young male, and older male during paced breathing at 0.25 Hz.

Beat-to-beat arterial pressure was estimated from the middle phalanx of the middle finger of the left hand with a photoplethysmograph (Finapres, model 2300, Ohmeda). This device has been validated for power spectral analysis of arterial pressure variability (32). Brachial arterial pressure also was measured with an oscillometric device (Dynamap, Critikon) or an auscultatory sphygmomanometer on the right arm immediately before the 5-min measurement period. These pressure readings were used to confirm the Finapres-derived arterial pressures. Respiratory excursions were measured by inductive plethysmography (Respitrace, Ambulatory Monitoring). Multiunit postganglionic muscle sympathetic nerve activity was measured via a tungsten microelectrode inserted into the right peroneal nerve near the fibular head, as previously described (49). The raw nerve signal was amplified, rectified, and integrated before recording (Nerve Traffic Analyzer, model 662c-3, University of Iowa Bioengineering). Recordings of muscle sympathetic nerve activity were confirmed by the relation of nervous activity to the cardiac cycle and to respiratory activity.

Data analysis and statistics. The electrocardiogram, respiration, beat-to-beat arterial pressure, and muscle sympathetic activity waveforms were digitized at 500 samples/s for off-line analysis with signal-processing software (CODAS, Dataq Instruments; DADiSP, DSP Development). R-R intervals, arterial pressures, and muscle sympathetic activity corresponding to nonsinus beats were eliminated; no subject demonstrated more than two nonsinus beats during the 5-min recording period. R-R intervals were derived from the time difference between marks placed on the peak of the R waves. Systolic and diastolic pressures were derived from the maximum and minimum of the beat-to-beat pressure waveform.

Average sympathetic outflow and sympathetic oscillations were calculated with the sympathetic neurogram standardized for burst height. The largest sympathetic burst occurring during the measurement period was assigned a value of 1,000 arbitrary integration units (aiu) for each subject; all other bursts were calibrated against that standard (49). This procedure eliminates the confound of electrode position on burst height; the voltage amplitude of multifiber sympathetic activity is critically dependent on the position of the electrode relative to the fibers. This is an important consideration for spectral analysis of sympathetic oscillations; differences in spectral power of uncalibrated recordings could result merely from closer electrode placement. Thus normalization of burst amplitude allows group comparisons for both total activity and oscillation amplitude of sympathetic outflow. Subsequently, muscle sympathetic nerve activity was quantified by custom-made programs designed to identify sympathetic bursts above baseline noise with the appropriate delay from the R wave of the electrocardiogram (~1.3 s; Ref. 10). Only bursts with a signal-to-noise ratio >2:1 were included for analysis, and noise artifacts were identified and manually edited from the analysis. For calculation of average muscle sympathetic activity, the area under each burst was measured, and the average burst area was derived for each subject. Average muscle sympathetic nerve activity was calculated as a function of time both as bursts per minute and as total activity (average burst area × bursts/min).

Average R-R interval and systolic and diastolic pressures were calculated from beat-to-beat values for each subject. Frequency domain analysis of variability was performed on beat-to-beat R-R intervals and beat-to-beat arterial pressures and on the respiratory and muscle sympathetic nerve activity waveforms. A power spectrum analysis technique based on the Welch algorithm of averaging periodograms was used (50). To obtain equidistant time intervals, the 300-s time series of beat-to-beat R-R intervals and arterial pressures were interpolated at 5 Hz, and the time series of respiratory and muscle sympathetic nerve activity waveforms were decimated to 5 Hz. Each time series was divided into five equal overlapping segments, detrended, Hanning filtered, and fast Fourier transformed to its frequency representation squared. The periodograms were averaged to produce the spectrum estimate. This method yielded a frequency resolution of 0.001 Hz. The areas under the power spectra in the Mayer wave and respiratory frequencies (defined as 0.05-0.15 and 0.20-0.30 Hz) were integrated and used for statistical comparisons. Relative (normalized) units were not used for comparisons of cardiovascular variabilities, since normalization produces unreliable estimates of power (47) and artificially generates an antipodal relation between the two primary oscillations (i.e., as one increases, the other must decrease; Ref. 9).

Coherence between fluctuations in muscle sympathetic nerve activity and arterial pressure was assessed by cross-spectral analysis based on models previously described (7, 8). For our coherence estimates, values exceeding 0.5 (range 0-1) represent a statistically reliable relation between the variabilities in the two signals at P = 0.10 (50). The coherence between fluctuations in muscle sympathetic nerve activity and both systolic and diastolic pressure Mayer waves were examined.

Group differences in time domain variables (e.g., average R-R interval, average arterial pressures) were assessed by Student's unpaired t-test. Group differences in variability data were assessed by Student's unpaired t-test after log transformation to achieve normal distribution and equal variance. Spearman rank-order correlations were used to assess the association between arterial pressure Mayer wave amplitude and average sympathetic activity and sympathetic nerve oscillations. A significance level of P < 0.05 was used. Data are presented as means ± SE.

    RESULTS
Top
Abstract
Introduction
Methods
Results
Discussion
References

Subjects controlled respiration very well throughout the 5-min measurement period; the majority of respiratory power was between 0.20 and 0.30 Hz in all subjects (93.5 ± 0.7%). Average R-R interval did not differ among the three groups (Table 1). There were no gender-related differences in R-R interval variability at either respiratory or low frequencies (Table 2). However, R-R interval variability in the respiratory and low frequencies was 87 and 83% lower in older males vs. young males (P < 0.05).

                              
View this table:
[in this window]
[in a new window]
  		Table 1.   Mean values for R-R interval, arterial pressures, and muscle sympathetic nerve activity during 5-min paced breathing at 0.25 Hz in 3 groups

                              
View this table:
[in this window]
[in a new window]
  		Table 2.   Low and respiratory frequency variability in R-R interval, arterial pressures, and muscle sympathetic nerve activity during 5-min paced breathing at 0.25 Hz in 3 groups

Average arterial pressures were not different in the three groups. There were marked gender- and age-related differences in average muscle sympathetic nerve activity calculated as either total activity per minute or bursts per minute. Total sympathetic nerve activity in the young females was only 36% of the activity in the young males whose sympathetic activity was, in turn, 31% lower than the activity in the older males (all P < 0.05; Table 1). There were no gender- or age-related differences in respiratory frequency variability in either systolic or diastolic pressure. However, both the young females and older males demonstrated less respiratory frequency variability in muscle sympathetic activity than the young males (P < 0.05; Table 2).

The striking gender- and age-related differences in average sympathetic outflow were not paralleled by similar differences in Mayer wave amplitude (Fig. 2). In fact, neither systolic nor diastolic pressure Mayer wave amplitude was different in the young females and males. Moreover, although an age-related difference in Mayer wave amplitude was apparent, it was not analogous to that in average sympathetic activity; despite greater sympathetic outflow, the older males had 60% less diastolic pressure variability in the low frequency than the young males (P < 0.05). Differences in the amplitude of sympathetic oscillations at the Mayer wave frequency were also inconsistent with group differences in Mayer wave amplitude. Both young females and older males had lower sympathetic oscillations at the Mayer wave frequency than the young males (both P < 0.05; Fig. 2).


View larger version (23K):
[in this window]
[in a new window]
  		Fig. 2.   Mayer wave amplitude in systolic pressure and diastolic pressure (A) and muscle sympathetic nerve activity (B) in young females, young males, and older males. aiu, Arbitrary integration units. * P < 0.05 vs. young males. dagger  P < 0.05 vs. young females.

Neither systolic nor diastolic Mayer wave amplitude was predictive of average sympathetic activity (Fig. 3); across all subjects and within each group, the correlation coefficient did not exceed 0.37 (all P > 0.20). There was also no relation between the sympathetic low-frequency oscillations and average sympathetic outflow (all r < 0.40). However, the Mayer wave oscillations in arterial pressure and sympathetic outflow were related both within individual subjects and within two of the three subject groups. The within-subject analogy to the correlation statistic, coherence, indicated a significant relation between Mayer wave oscillations in arterial pressure and sympathetic outflow in >90% of the subjects. Coherence between systolic pressure and sympathetic activity averaged 0.60 in all subjects with only 5 of 34 subjects below 0.50, and that between diastolic pressure and sympathetic activity averaged 0.61 with 4 of 34 subjects below 0.50. The subjects without significant coherence were equally distributed across the three groups. Thus a strong frequency domain relation between arterial pressure and sympathetic activity at the Mayer wave frequency existed within a majority of subjects. Despite this, only the male subject groups demonstrated any correlation between the amplitudes of sympathetic and arterial pressure oscillations (Fig. 4). Interestingly, systolic pressure Mayer waves were negatively related to sympathetic oscillations in the young group, whereas arterial pressure Mayer waves were positively related in the older group (Fig. 4, and diastolic r = 0.62, P < 0.05). However, these correlations indicate that only 34-40% of the variability in Mayer wave amplitude can be accounted for by sympathetic Mayer wave oscillations. Thus arterial pressure Mayer waves did not reflect sympathetic outflow reliably across groups and only marginally reflected sympathetic oscillations in the two male groups.


View larger version (16K):
[in this window]
[in a new window]
  		Fig. 3.   Scatter plots of relations between average sympathetic activity and Mayer wave amplitude in systolic (A) and diastolic pressures (B) in all subjects.


View larger version (19K):
[in this window]
[in a new window]
  		Fig. 4.   Scatter plots of relations between sympathetic and systolic pressure oscillations at Mayer wave frequency in each group. Correlation coefficients and significance levels are indicated for each relation.

    DISCUSSION
Top
Abstract
Introduction
Methods
Results
Discussion
References

These results indicate that arterial pressure Mayer wave amplitude does not provide a surrogate measure for vascular sympathetic outflow. There was no proportionality between arterial pressure Mayer wave amplitude and average sympathetic activity across three groups with markedly different sympathetic outflow. Although a modest relation between Mayer waves and sympathetic oscillations was evident in the young and older males, it was highly inconsistent between these two groups. Even broad examination of gender- and age-related differences does not provide convincing evidence for exclusive sympathetic mediation of arterial pressure Mayer waves. Lower sympathetic nerve activity and lower sympathetic oscillations at the Mayer wave frequency did not correspond to smaller arterial pressure Mayer waves in the young females. In contrast, higher sympathetic nerve activity and lower sympathetic oscillations at the Mayer wave frequency did correspond to smaller arterial pressure Mayer waves in the older males. The juxtaposition of these findings underscores the fundamental complexity of cardiovascular variabilities and their limitations as convenient markers of autonomic outflow.

Significance of Mayer wave oscillations. Although respiratory frequency arterial pressure variability derives, in part, from mechanical effects of respiratory sinus arrhythmia, arterial pressure Mayer waves do not originate from heart rate oscillations in the low frequency (31, 47). Mayer waves are most apparent in response to sympathoexcitatory stimuli (26), and coherence between arterial pressure and sympathetic activity at the Mayer wave frequency has been shown in both the present and previous studies (21, 33, 36). Thus a reasonable conclusion is that waxing and waning vascular resistance because of sympathetic neural oscillations generates arterial pressure Mayer waves (1, 8, 11, 14, 15, 25, 37). This construct underlies two premises for the use of Mayer wave amplitude as an index of autonomic function. Because a sympathetic effector has been presumed a prerequisite for arterial pressure Mayer waves (16) and some studies have found that alpha -receptor blockade (4, 20) or spinal cord injury (18) eliminates Mayer waves, low-frequency arterial pressure variability has been identified as an index of vascular sympathetic outflow (12, 24, 27, 33, 38). Furthermore, because the arterial baroreflex may be a key component for sympathetic oscillations (5, 8, 15, 25) and some data suggest that Mayer waves are dependent on intact arterial baroreflex function (3, 45), it has been proposed that Mayer wave amplitude is proportional to baroreflex gain (8, 45). Although both are based on reasonable evidence, neither premise accounts for countervailing influences on Mayer wave amplitude.

We found that mean levels of vascular sympathetic outflow and Mayer wave amplitude are not proportional. These findings indicate that low-frequency arterial pressure variability should not be identified as an index of vascular sympathetic outflow. Indeed, the exact relation between mean sympathetic outflow and Mayer wave amplitude is unclear. Although acute sympathetic ganglionic blockade reduces low-frequency arterial pressure variability in both humans (43) and rats (3), some patients with high spinal transection demonstrate clearly identifiable Mayer waves (16, 22), and rats after chemical sympathectomy demonstrate increased low-frequency arterial pressure variability (6). Thus it appears that Mayer waves can be generated by mechanisms other than sympathetically mediated vasoconstriction, such as autochthonous vascular smooth muscle contractions (44).

We did not find that arterial pressure Mayer wave amplitude was correlated with sympathetic oscillations at the Mayer wave frequency in all subjects. This finding brings into question the idea that arterial pressure Mayer waves are reflective of baroreflex gain (8, 45). If the classical concept of arterial baroreflex gain (42) is extrapolated to interindividual differences in cardiovascular variabilities, then oscillations in arterial pressure input should be comparable to oscillations in baroreflex-mediated sympathetic output. Although this relation did not maintain across all subjects, it did maintain within most subjects. The high coherence between low-frequency sympathetic and arterial pressure oscillations in most subjects may denote a baroreflex link. However, our data indicate that similar sympathetic outflow at the Mayer wave frequency may generate different levels of arterial pressure oscillations; our young females and older males had striking differences in Mayer wave amplitude with similar low-frequency sympathetic oscillations. Thus our results suggest that Mayer wave amplitude is influenced importantly by factors other than baroreflex gain.

Our findings support the observations of Stauss et al. (46). They found no relations between arterial pressure Mayer waves and either the mean level or the Mayer wave oscillations of splanchnic sympathetic nervous outflow in rats. However, our findings are in contrast to the only previous data in humans. Pagani et al. (33) found very high significance levels (P = 0.00001-0.04) of regressions between arterial pressure Mayer waves, average sympathetic nervous outflow, and sympathetic nervous oscillations in young males. Nonetheless, the significance levels did not relate to a high predictive power; calculated correlation coefficients for their data show values that do not exceed 0.46. Thus the only previous data in humans support our findings of no relation between arterial pressure Mayer waves and average sympathetic outflow and only a limited relation between arterial pressure Mayer waves and sympathetic oscillations.

Gender- and age-related differences. There is some previous data on gender- and age-related differences in arterial pressure Mayer waves. There is one report of lower systolic pressure variability in women compared with men (41), yet we found no gender-related difference in our young subjects. A previous comparison of healthy older and young subjects found an age-related reduction in both systolic and diastolic Mayer wave amplitude (48). Although we found systolic Mayer wave amplitude was >20% lower, only diastolic Mayer wave amplitude was statistically lower in the older compared with the young men. Disagreement between the present and previous findings may be because of methodological differences; gender- and age-related differences in the previous studies were only evident during spontaneous breathing. Breathing frequency has profound impact on arterial pressure variability, in part through changes in respiratory sinus arrhythmia (23). Furthermore, respiratory-related heart rate variability augments systolic more than diastolic pressure (47). Thus previously reported gender- and age-related differences in systolic Mayer wave amplitude may be merely because of slow breathing frequencies in female and older subjects.

The lack of intergroup correlations and the discrepant intragroup relations between sympathetic outflow and arterial pressure Mayer waves indicate that no single mechanism explains gender- or age-related differences. However, there may be factors that alter vascular responsiveness to sympathetic activity and that underlie general differences in the relations among arterial pressure Mayer waves, mean sympathetic activity, and sympathetic outflow oscillations. Gender-related differences could derive from the effects of estrogen on vascular smooth muscle (13). Estrogen enhances flow-dependent nitric oxide release (40), which has been shown to diminish arterial pressure oscillations (29, 35). However, our findings of similar oscillations in young females and males are contrary to this effect. Gender- and age-related differences in levels of and sensitivity to angiotensin (19) could define the relations between arterial pressure oscillations and sympathetic outflow; angiotensin is a powerful vasoconstrictive that may alter the vascular responsiveness to adrenergic stimulation. However, acute angiotensin blockade does not alter arterial pressure Mayer waves in young males and females (2), although it may have more significant effects on Mayer waves in older humans. Reduced sensitivity of alpha -receptors on vascular smooth muscle with age has been reported (17), which would decrease the arterial pressure response to sympathetic outflow, yet we found a direct relation between the amplitude of sympathetic outflow oscillations and arterial pressure Mayer waves in our older males. The structural conduit for Mayer waves is the arterial vasculature; thus arterial stiffness may be a prime component of differences in the relation between sympathetic outflow oscillations and Mayer wave amplitude. Although there are no analogous gender-related data, vascular stiffness does increase profoundly with age (39). Although this may explain lower Mayer waves in older men, it is likely that the striking age-related difference in the relation between Mayer wave oscillations in arterial pressure and sympathetic outflow is multifactorial.

Study limitations. Our young females were not examined at a consistent point in the menstrual cycle; thus the lack of correlation between arterial pressure and sympathetic oscillations in this group may have been secondary to variable hormonal status. Nonetheless, this supports our contention that large intersubject variability precludes the use of arterial pressure Mayer waves as a simple marker for vascular sympathetic outflow. Although these data elucidate cross-sectional differences in arterial pressure and sympathetic activity Mayer wave oscillations, they do not inform the proportionality between sympathetic outflow and Mayer waves within individuals. It is unknown if Mayer wave relations are maintained under changing conditions within subjects. If these relations are stable within subjects, Mayer waves could be a valid comparator for cardiovascular autonomic control. However, this seems improbable; present findings of marked subject-to-subject variability and previous findings of the mutable links between cardiovascular variabilities (47) indicate that Mayer waves likely have myriad effectors and are not only secondary to baroreflex-mediated sympathetic outflow.

Conclusions. Understanding arterial pressure variability may have clinical application, since the magnitude of variability is related to morbid events including cardiac ischemia and heart failure (34). However, our results demonstrate that Mayer wave amplitude does not reflect mean sympathetic activity. Moreover, the relations we found between Mayer wave frequency oscillations in arterial pressure and sympathetic activity were evident only within specific groups and were inconsistent between those groups. Thus it appears that Mayer waves may be generated and influenced by a myriad of factors other than sympathetically mediated vasoconstriction and/or baroreflex gain. Our data underscore the fundamental complexity of cardiovascular variabilities and their limitations as convenient markers of autonomic outflow.

    ACKNOWLEDGEMENTS

This research was supported by the American Federation for Aging Research; National Institute on Aging Grants AG-14226-01, AG-06537, and AG-00687; and the Colorado American Heart Association.

    FOOTNOTES

Address for reprint requests: J. A. Taylor, Laboratory for Cardiovascular Research, HRCA Research and Training Institute, 1200 Centre St., Boston, MA 02131.

Received 10 July 1997; accepted in final form 17 December 1997.

    REFERENCES
Top
Abstract
Introduction
Methods
Results
Discussion
References

1.   Basselli, G., S. Cerutti, S. Civardi, A. Malliani, and M. Pagani. Cardiovascular variability signals: toward the identification of a closed-loop model of the neural mechanisms. IEEE Trans. Biomed. Eng. 35: 1033-1046, 1988[Medline].

2.   Carr, D. E., J. A. Taylor, and D. L. Eckberg. Autonomic mechanisms responsible for very low frequency R-R interval oscillations (Abstract). FASEB J. 9: A126, 1995.

3.   Cerutti, C., C. Barres, and C. Paultre. Baroreflex modulation of blood pressure and heart rate variabilities in rats: assessment by spectral analysis. Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H1993-H2000, 1994[Abstract/Free Full Text].

4.  Clement, D. L., M. D. Buyzere, and D. D. Duprez. Influence of drugs on blood pressure variability. J. Hypertens. 12, Suppl.: S49-S53, 1994.

5.   Craelius, W., V. K. H. Chen, M. Restivo, and N. El-Sherif. Rhythm analysis of arterial blood pressure. IEEE Trans. Biomed. Eng. 33: 1166-1172, 1986[Medline].

6.   Daffonchio, A., C. Franselli, A. Radaelli, P. Castiglioni, M. D. Rienzo, G. Manzia, and A. U. Ferrari. Sympathectomy and cardiovascular spectral components in conscious normotensive rats. Hypertension 25: 1287-1293, 1995[Abstract/Free Full Text].

7.   DeBoer, R. W., J. M. Karemaker, and J. Strackee. Relationships between short-term blood-pressure fluctuations and heart-rate variability in resting subjects. I. A spectral analysis approach. Med. Biol. Eng. Comp. 23: 352-358, 1985[Medline].

8.   DeBoer, R. W., J. M. Karemaker, and J. Strackee. Hemodynamic fluctuations and baroreflex sensitivity in humans. Am. J. Physiol. 253 (Heart Circ. Physiol. 22): H680-H689, 1987[Abstract/Free Full Text].

9.   Eckberg, D. L. Sympathovagal balance: a critical appraisal. Circulation 96: 3224-3232, 1997[Free Full Text].

10.   Fagius, J., and B. G. Wallin. Sympathetic reflex latencies and conduction velocities in normal man. J. Neurol. Sci. 47: 433-448, 1980[Medline].

11.   Fredericq, L. De l'influence de la respiration sur la circulation. Arch. Biol. 3: 55-100, 1887.

12.   Furlan, R., S. Guzzetti, W. Crivellaro, S. Dassi, M. Tinelli, G. Baselli, S. Cerutti, F. Lombardi, M. Pagani, and A. Malliani. Continuous 24-hour assessment of the neural regulation of systemic arterial pressure and RR variabilities in ambulant subjects. Circulation 81: 537-547, 1990[Abstract/Free Full Text].

13.   Gilligan, G. M., D. M. Badar, J. A. Panza, A. A. Quyyumi, and R. O. Cannon. Acute vascular effects of estrogen in postmenopausal women. Circulation 90: 786-791, 1994[Abstract/Free Full Text].

14.   Green, H. D., R. N. Lewis, and N. D. Nickerson. Quantification of changes in vasomotor tone: change of vasomotor tone as cause of Traube Hering waves. Proc. Soc. Exp. Biol. Med. 53: 228-229, 1943.

15.   Guyton, A. C., H. M. Batson, C. M. Smith, and G. G. Armstrong. Method for studying competence of the body's blood pressure regulatory mechanisms and effect of pressoreceptor denervation. Am. J. Physiol. 164: 360-368, 1951.

16.   Guzzetti, S., C. Cogliati, C. Broggi, C. Carozzi, D. Caldiroli, F. Lombardi, and A. Malliani. Influences of neural mechanisms on heart period and arterial pressure variabilities in quadriplegic patients. Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H1112-H1120, 1994[Abstract/Free Full Text].

17.   Hogikyan, R. V., and M. A. Supiano. Arterial alpha-adrenergic responsiveness is decreased and SNS activity is increased in older humans. Am. J. Physiol. 266 (Endocrinol. Metab. 29): E717-E724, 1994[Abstract/Free Full Text].

18.   Inoue, K., S. Miyake, M. Kumashiro, H. Ogata, T. Ueta, and T. Akatsu. Power spectral analysis of blood pressure variability in traumatic quadriplegic humans. Am. J. Physiol. 260 (Heart Circ. Physiol. 29): H842-H847, 1991[Abstract/Free Full Text].

19.   Ishibashi, K., T. Oshima, H. Matsuura, M. Watanabe, M. Ishida, T. Ishida, R. Ozono, G. Kajiyama, and M. Kanbe. Effects of age and sex on sodium chloride sensitivity: association with plasma renin activity. Clin. Nephrol. 42: 376-380, 1994[Medline].

20.   Japundzic, N., M. L. Grichois, P. Zitoun, D. Laude, and J. L. Elghozi. Spectral analysis of blood pressure and heart rate in conscious rats: effects of autonomic blockers. J. Auton. Nerv. Syst. 30: 91-100, 1990[Medline].

21.   Kaminski, R. J., G. A. Meyer, and D. L. Winter. Sympathetic unit activity associated with Mayer waves in the spinal dog. Am. J. Physiol. 219: 1768-1771, 1970.

22.   Koh, J., T. E. Brown, L. A. Beightol, C. Y. Ha, and D. L. Eckberg. Human autonomic rhythms: vagal cardiac mechanisms in tetraplegic subjects. J. Physiol. (Lond.) 474: 483-495, 1994[Abstract/Free Full Text].

23.   Laude, D., M. Goldman, P. Escourrou, and J. L. Elghozi. Effect of breathing pattern on blood pressure and heart rate oscillations in humans. Clin. Exp. Pharmacol. Physiol. 20: 619-626, 1993[Medline].

24.   Lipsitz, L. A., C. M. Connelly, M. Kelley-Gagnon, D. K. Kiely, and R. J. Morin. Effects of chronic estrogen replacement therapy on beat-to-beat pressure dynamics in healthy postmenopausal women. Hypertension 26: 711-715, 1995[Abstract/Free Full Text].

25.   Madwed, J. B., P. Albrecht, R. G. Mark, and R. J. Cohen. Low-frequency oscillations in arterial pressure and heart rate: a simple computer model. Am. J. Physiol. 256 (Heart Circ. Physiol. 25): H1573-H1579, 1989[Abstract/Free Full Text].

26.   Madwed, J. B., and R. J. Cohen. Heart rate response to hemorrhage-induced 0.05-Hz oscillations in arterial pressure in conscious dogs. Am. J. Physiol. 260 (Heart Circ. Physiol. 29): H1248-H1253, 1991[Abstract/Free Full Text].

27.   Malliani, A., M. Pagani, F. Lombardi, and S. Cerutti. Clinical and experimental evaluation of sympathovagal interaction: power spectral analysis of heart rate and arterial pressure variabilities. In: Reflex Control of the Circulation. Boca Raton, FL: CRC, 1991, p. 937-964.

28.   Mayer, S. Studien zur Physiologie des Herzens und der Blutgefasse: 5. Abhandlung: Uber spontane Blutdruckschwankungen. Sber. Akad. Wiss. Wien. 74: 281-307, 1876.

29.   Nafz, B., A. Just, H. M. Stauss, C. D. Wagner, H. Ehmke, H. R. Kirchheim, and P. B. Persson. Blood-pressure variability is buffered by nitric oxide. J. Auton. Nerv. Syst. 57: 181-183, 1996[Medline].

30.   Ng, A. V., R. Callister, D. G. Johnson, and D. R. Seals. Age and gender influence muscle sympathetic nerve activity at rest in healthy humans. Hypertension 21: 498-503, 1993[Abstract/Free Full Text].

31.   O'Leary, D. S., and D. J. Woodbury. Role of cardiac output in mediating arterial blood pressure oscillations. Am. J. Physiol. 271 (Regulatory Integrative Comp. Physiol. 40): R641-R646, 1996[Abstract/Free Full Text].

32.   Omboni, S., G. Parati, A. Frattola, E. Mutti, M. D. Rienzo, P. Castiglioni, and G. Mancia. Spectral and sequence analysis of finger blood pressure variability: comparison with analysis of intra-arterial recordings. Hypertension 22: 26-33, 1993[Abstract/Free Full Text].

33.   Pagani, M., N. Montano, A. Porta, A. Malliani, F. M. Abboud, C. Birkett, and V. K. Somers. Relationship between spectral components of cardiovascular variabilities and direct measures of muscle sympathetic nerve activity in humans. Circulation 95: 1441-1448, 1997[Abstract/Free Full Text].

34.   Palatini, P., M. Penzo, A. Racioppa, E. Zugno, G. Guzzardi, M. Anaclerio, and A. C. Pessina. Clinical relevance of nighttime blood pressure and of daytime blood pressure variability. Arch. Intern. Med. 152: 1855-1860, 1992[Abstract].

35.   Persson, P. B., J. E. Baumann, H. Ehmke, B. Nafz, U. Wittmann, and H. R. Kirchheim. Phasic and 24-h blood pressure control by endothelium-derived relaxing factor in conscious dogs. Am. J. Physiol. 262 (Heart Circ. Physiol. 31): H1395-H1400, 1992[Abstract/Free Full Text].

36.   Persson, P. B., H. Stauss, O. Chung, U. Wittmann, and T. Unger. Spectrum analysis of sympathetic nerve activity and blood pressure in conscious rats. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1348-H1355, 1992[Abstract/Free Full Text].

37.   Preiss, G., and C. Polosa. Patterns of sympathetic neuron activity associated with Mayer waves. Am. J. Physiol. 226: 724-730, 1974.

38.   Radaelli, A., L. Bernardi, F. Valle, S. Leuzzi, F. Salvucci, L. Pedrotti, E. Marchesi, G. Finardi, and P. Sleight. Cardiovascular autonomic modulation in essential hypertension: effect of tilting. Hypertension 24: 556-563, 1994[Abstract/Free Full Text].

39.   Reneman, R. S., T. V. Merode, P. Hick, A. M. M. Muytjens, and A. P. G. Hoeks. Age-related changes in carotid artery wall properties in men. Ultrasound Med. Biol. 12: 465-471, 1986[Medline].

40.   Rosselli, M., B. Imthurn, P. J. Keller, E. K. Jackson, and R. K. Dubey. Circulating nitric oxide (nitrite/nitrate) levels in postmenopausal women substituted with 17beta -estradiol and norethisterone acetate: a two-year follow-up study. Hypertension 25: 848-853, 1995[Abstract/Free Full Text].

41.  Ryan, S. M., L. A. Lipsitz, and A. L. Goldberger. Importance of gender in spectral analysis of blood pressure dynamics (Abstract). Circulation 86, Suppl. I: I-586, 1992.

42.   Sagawa, K. Concerning "gain." Am. J. Physiol. 235 (Heart Circ. Physiol. 4): H117, 1978.

43.   Scheffer, G. J., B. J. TenVoorde, J. M. Karemaker, and H. H. Ros. Effects of epidural analgesia and atropine on heart rate and blood pressure variability: implications for the interpretation of beat-to-beat fluctuations. Eur. J. Anaesthesiol. 11: 75-80, 1994[Medline].

44.   Seigal, G., A. Adler, B. J. Ebeling, H. Roedel, H. W. Hofer, and J. Nolte. Temporal behaviour of transmembrane ion exchange in vascular smooth muscle. Circ. Res. 72: 440-454, 1984[Abstract/Free Full Text].

45.   Sleight, P., T. L. Rovere, A. Mortara, G. Pinna, R. Maestri, S. Leuzzi, B. Bianchini, L. Tavazzi, and L. Bernardi. Physiology and pathophysiology of heart rate and blood pressure variability in humans: is power spectral analysis largely an index of baroreflex gain? Clin. Sci. 88: 103-109, 1995[Medline].

46.   Stauss, H. M., R. Mrowka, B. Nafz, A. Patzak, T. Unger, and P. B. Persson. Does low frequency power of arterial blood pressure reflect sympathetic tone? J. Auton. Nerv. Syst. 54: 145-154, 1995[Medline].

47.   Taylor, J. A., and D. L. Eckberg. Fundamental relations between short-term R-R interval and arterial pressure oscillations in humans. Circulation 93: 1527-1532, 1996[Abstract/Free Full Text].

48.   Veerman, D. P., P. M. Imholz, W. Wieling, J. M. Karemaker, and G. A. V. Montfrans. Effects of aging on blood pressure variability in resting conditions. Hypertension 24: 120-130, 1994[Abstract/Free Full Text].

49.   Wallin, B. G., and D. L. Eckberg. Sympathetic transients caused by abrupt alterations of baroreceptor activity in man. Am. J. Physiol. 242 (Heart Circ. Physiol. 11): H185-H190, 1982.

50.   Welch, P. D. The use of fast Fourier transform for the estimation of power spectra: a method based on time averaging over short, modified periodograms. IEEE Trans. Audio. Electroacoust. 15: 70-73, 1967.

AJP Heart Circ Physiol 274(4):H1194-H1201
0363-6135/98 $5.00 Copyright © 1998 the American Physiological Society


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
I. Krabbendam, L. C. A. Jacobs, F. K. Lotgering, and M. E. A. Spaanderman
Venous response to orthostatic stress
Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1587 - H1593.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
J. Cui, S. Durand, and C. G. Crandall
Baroreflex control of muscle sympathetic nerve activity during skin surface cooling
J Appl Physiol, October 1, 2007; 103(4): 1284 - 1289.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
M. Ichinose, S. Koga, N. Fujii, N. Kondo, and T. Nishiyasu
Modulation of the spontaneous beat-to-beat fluctuations in peripheral vascular resistance during activation of muscle metaboreflex
Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H416 - H424.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
S. C. Aslan, D. C. Randall, K. D. Donohue, C. F. Knapp, A. R. Patwardhan, S. M. McDowell, R. F. Taylor, and J. M. Evans
Blood pressure regulation in neurally intact human vs. acutely injured paraplegic and tetraplegic patients during passive tilt
Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1146 - R1157.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
G. Parati, G. Mancia, M. D. Rienzo, P. Castiglioni, J. A. Taylor, and P. Studinger
Point:Counterpoint: Cardiovascular variability is/is not an index of autonomic control of circulation
J Appl Physiol, August 1, 2006; 101(2): 676 - 682.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
J. Cui, M. Sathishkumar, T. E. Wilson, M. Shibasaki, S. L. Davis, and C. G. Crandall
Spectral characteristics of skin sympathetic nerve activity in heat-stressed humans
Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1601 - H1609.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
C. M. Foley, P. J. Mueller, E. M. Hasser, and C. M. Heesch
Hindlimb unloading and female gender attenuate baroreflex-mediated sympathoexcitation
Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2005; 289(5): R1440 - R1447.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
Y. Chen, L. F. Joaquim, V. M. Farah, R. B. Wichi, R. Fazan Jr., H. C. Salgado, and M. Morris
Cardiovascular autonomic control in mice lacking angiotensin AT1a receptors
Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2005; 288(4): R1071 - R1077.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
D. D. O'Leary, J. K. Shoemaker, M. R. Edwards, and R. L. Hughson
Spontaneous beat-by-beat fluctuations of total peripheral and cerebrovascular resistance in response to tilt
Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2004; 287(3): R670 - R679.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
J. Cui, R. Zhang, T. E. Wilson, and C. G. Crandall
Spectral analysis of muscle sympathetic nerve activity in heat-stressed humans
Am J Physiol Heart Circ Physiol, March 1, 2004; 286(3): H1101 - H1106.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
W. H. Cooke, G. L. Pellegrini, and O. A. Kovalenko
Dynamic cerebral autoregulation is preserved during acute head-down tilt
J Appl Physiol, October 1, 2003; 95(4): 1439 - 1445.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
W. H. Cooke, R. Zhang, J. H. Zuckerman, J. Cui, T. E. Wilson, C. G. Crandall, and B. D. Levine
Does nitric oxide buffer arterial blood pressure variability in humans?
J Appl Physiol, October 1, 2002; 93(4): 1466 - 1470.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
D. W. Wray, K. J. Formes, M. S. Weiss, A. H. O-Yurvati, P. B. Raven, R. Zhang, and X. Shi
Vagal cardiac function and arterial blood pressure stability
Am J Physiol Heart Circ Physiol, November 1, 2001; 281(5): H1870 - H1880.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
J. K. Shoemaker, C. S. Hogeman, M. Khan, D. S. Kimmerly, and L. I. Sinoway
Gender affects sympathetic and hemodynamic response to postural stress
Am J Physiol Heart Circ Physiol, November 1, 2001; 281(5): H2028 - H2035.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
J. W. Hamner and J. A. Taylor
Automated quantification of sympathetic beat-by-beat activity, independent of signal quality
J Appl Physiol, September 1, 2001; 91(3): 1199 - 1206.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
D. Mestivier, H. Dabire, and N. P. Chau
Effects of autonomic blockers on linear and nonlinear indexes of blood pressure and heart rate in SHR
Am J Physiol Heart Circ Physiol, September 1, 2001; 281(3): H1113 - H1121.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
F. Yasuma and J.-I. Hayano
Augmentation of respiratory sinus arrhythmia in response to progressive hypercapnia in conscious dogs
Am J Physiol Heart Circ Physiol, May 1, 2001; 280(5): H2336 - H2341.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
F. Yasuma and J.-I. Hayano
Impact of acute hypoxia on heart rate and blood pressure variability in conscious dogs
Am J Physiol Heart Circ Physiol, November 1, 2000; 279(5): H2344 - H2349.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
J. A. Taylor, C. W. Myers, N. Montano, C. Cogliati, A. Porta, M. Pagani, A. Malliani, K. Narkiewicz, F. M. Abboud, and V. K. Somers
Mathematical Treatment of Autonomic Oscillations - 2 • Response
Circulation, October 12, 1999; 100 (15): e64 - e64.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow