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1 Department of Cardiology/Hypertension Clinic, Erasme Hospital, 1070 Brussels, Belgium; 2 Centro Ricerche Cardiovascolari, Consiglio Nazionale delle Ricerca, Dipartimento di Scienze Precliniche Laboratorio Interdisciplinare Technologie Avanzare di Vialba, Medicina Interna II, Ospedale L. Sacco, Università degli studi di Milano, 20157 Milano, Italy; and 3 Hypertension and Cardiovascular Divisions, Mayo Clinic, Rochester, Minnesota 55902
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ABSTRACT |
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 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The relative contributions of a
central neural oscillator and of the delay in 
-adrenergic
transmission within the baroreflex loop in the predominance of
low-frequency (LF) cardiovascular variability during sympathetic
activation in humans are unclear. We measured R-R interval (RR), muscle
sympathetic nerve activity (MSNA), blood pressure (BP), and their
variability in 10 normal subjects during sympathetic activation
achieved by BP lowering with sodium nitroprusside (SNP) and
-adrenergic blockade using phentolamine. SNP and phentolamine
induced comparable reductions in BP (P > 0.25).
Despite tachycardia and sympathetic activation with both SNP and
phentolamine, LF variability in RR, MSNA, and BP increased during SNP
and decreased during phentolamine (SNP: RR +20 ± 6%, MSNA
+3 ± 5%, systolic BP +9 ± 6%, diastolic BP +7 ± 5%; phentolamine: RR 
2 ± 7%, MSNA 34 ± 6%, systolic
BP 16 ± 8%, diastolic BP 13 ± 4%, P < 0.05 except systolic BP, where P = 0.09). Thus LF
variability is reduced when sympathetic activation is induced by
-adrenergic blockade. This suggests that -adrenergic transmission
within the baroreflex loop may contribute importantly to the
predominance of LF cardiovascular variability associated with
sympathetic excitation in humans.
sympathetic nervous system
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INTRODUCTION |
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ABSTRACT
INTRODUCTION
METHODS
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DISCUSSION
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IN HEALTHY HUMANS, heart rate, blood pressure (BP), and muscle sympathetic nerve activity (MSNA) display low-frequency (LF) oscillations of ~0.10 Hz and faster oscillations at the respiratory frequency [high frequency (HF)] (28). The mechanisms underlying LF oscillations in human cardiovascular variability are not well understood. What is known is that, in closed-loop conditions, arterial baroreflex deactivation and the consequent sympathetic activation are accompanied by a relative enhancement of the LF oscillations in the variability patterns of heart rate, MSNA, and BP compared with the HF oscillations (27, 28).
There is evidence that a resonance phenomenon, due to delay in the
-adrenergic vasoconstrictor response mediated by the baroreceptors, contributes to the LF oscillations (2, 4-6, 9, 11).
However, LF components have also been reported in the absence of a
functional baroreflex loop. First, LF components were found in the
variability of the discharge of single medullary neurons
(24) and in sinoaortic denervated cats (25).
Second, oscillations in sympathetic nerve discharge synchronous with
BP, persist after high cervical spinal transection (12, 14, 21,
30). Third, substantial LF oscillations were found in R-R
interval (RR) variability of two subjects with left ventricular assist
devices, in whom the RR variability could not be attributed to the
minimal BP variability (7). Thus a functional baroreflex
loop may not be mandatory for the genesis of LF oscillations.
The relative contributions of a central neural oscillator and of the
delay in -adrenergic transmission within the baroreflex loop in the
predominance of LF cardiovascular variability during sympathetic
activation are not known in humans.
We anticipated that the analysis of the effect of sympathetic
activation, achieved by pharmacological BP lowering with -adrenergic blockade, on LF oscillations in MSNA might help to distinguish between
these mechanisms. -Adrenergic blockade decreases the LF variability
of BP in animals (8, 19, 20). However, this reduction
could be due to 1) the suppression of the LF variability in
MSNA as a result of the interruption of the baroreflex loop at the
neurovascular junction or 2) the interruption of transfer to
the vascular beds of an intrinsic increase in the LF power in MSNA
during sympathetic activation. Thus enhanced LF oscillations in MSNA
during -adrenergic blockade would suggest that the rise in LF
oscillations during sympathetic activation is mainly generated centrally. In contrast, reduction in LF oscillations in MSNA would suggest that -adrenergic transmission within the baroreflex loop contributes importantly to enhanced LF oscillatory power associated with sympathetic activation. We therefore determined changes in neural
and cardiovascular variability during BP reduction induced by
phentolamine (an -adrenergic receptor blocker) and compared these
changes with those induced by sodium nitroprusside (SNP; a direct
arterial and venous dilator). We further ensured the effectiveness of
-adrenergic blockade with phentolamine by examining the effects of
phenylephrine, an -agonist.
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METHODS |
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METHODS
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DISCUSSION
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Subjects. We studied 10 normal male subjects aged 30 ± 5 yr (range 22-38 yr). None were taking any medication. Informed written consent was obtained from all subjects. The Erasme Hospital Human Subjects Review Committee approved the study.
Measurements. Systolic (SBP) and diastolic BP (DBP) were measured every minute with a physiocontrol Colin BP-880 sphygmomanometer. Finger BP (Finapres), electrocardiogram (Siemens), and respiration (Respitrace) were recorded on a MacLab 8/s data acquisition system. Sympathetic nerve activity to muscle (MSNA) was recorded continuously by obtaining multiunit recordings of postganglionic sympathetic activity, measured from a nerve fascicle in the peroneal nerve posterior to the fibular head as described previously (10). Electrical activity in the nerve fascicle was measured using tungsten microelectrodes (shaft diameter 200 µm, tapering to an noninsulated tip of 1-5 µm). A subcutaneous reference electrode was inserted 2-3 cm away from the recording electrode, which was inserted into the nerve fascicle. The neural signals were amplified, filtered, rectified, and integrated to obtain a mean voltage display of sympathetic nerve activity.
Protocols and interventions.
The primary goal of the interventions was to induce comparable
baroreflex deactivation through similar BP reductions with SNP and
phentolamine. Measurements were taken during a baseline period of 10 min followed by an infusion of 0.8-1.5
µg · kg
1 · min1 SNP
during 10 min. This sequence was followed by a rest period of at least
15 min, and the next part of the study started only after heart rate
and BP had returned to initial baseline levels. Measurements were then
taken during another baseline period of 10 min followed by a period of
20 min, during which two boluses of 20 mg phentolamine were given at
10-min intervals. Phentolamine and SNP were administered on different
days in two subjects.
-adrenergic blockade with phentolamine was
verified in all 10 subjects using an infusion of 0.9 µg · kg1 · min1
phenylephrine. This infusion was started 10 min after the second bolus
of phentolamine and continued for 5 min. In 2 of 10 subjects, the
infusion of phenylephrine was repeated in the absence of phentolamine. This allowed us to determine the effects of phenylephrine on baseline cardiovascular parameters and to compare these effects with those induced by phenylephrine after the infusion of phentolamine. The effectiveness of -adrenergic blockade by phentolamine was further confirmed by studying the effects of 0.9 µg · kg1 · min1
phenyleprine on cardiovascular measures recorded during baseline conditions in four additional healthy volunteers.
Technically excellent studies examining the effects of phentolamine and
SNP on MSNA were obtained in 9 of 10 subjects. A loss of sympathetic
nerve recording occurred after the end of the phentolamine session in
one subject. Excellent recordings of the effects of phenylephrine on
MSNA after phentolamine were therefore obtained in 8 of 10 subjects.
Data analysis. Sympathetic bursts were identified by a careful inspection of the mean voltage neurogram. The amplitude of each burst was determined, and sympathetic activity was calculated as bursts per minute multiplied by the mean burst amplitude. Changes in MSNA were calculated as the percent change from baseline. A single observer (M. Rahnama) made measurements.
Analog-to-digital conversion was performed over 10 min at 300 sample/s for the electrocardiogram, BP, MSNA, and respiratory signals. The data were then analyzed off-line with a personal computer (IBM 433DX/T). The principles of the software for data acquisition and autoregressive spectral analysis have been described elsewhere (1, 23, 27, 28). The signal of MSNA was time integrated over each RR. SBP and DBP were determined in correspondence with the R wave while the signal of respiratory activity was sampled once every cardiac cycle. These procedures produced four time series (neurogram, systogram, diastogram, and respirogram), which were synchronized with the tachogram. Stationary segments devoid of arrhythmias and artifacts were analyzed with autoregressive algorithms by a single observer (S. Mezzetti). These algorithms automatically provide the number, center frequency, and power of the oscillatory components. Anderson's test (1) verified that all information contained in the time series had been extracted in the computation, and Akaike's test (1) allowed the determination of the optimal model order fitting the data. Previous studies (23, 27, 28, 32, 34) have shown that two major oscillatory components are detectable in short-term RR and MSNA and BP variability. One of these oscillatory components is synchronous with respiration and is called HF oscillation. The other component is described as LF oscillation and has a center frequency of ~0.10 Hz, but can vary considerably (from 0.04 to 0.15 Hz) (23, 27, 28, 34). In this study, the LF and HF components were expressed in normalized units. The normalized LF and HF units were obtained by calculating the absolute variability of each LF and HF component as a percentage of the total power after subtracting the power of the very LF component (frequencies below nominal 0.03 Hz) (23, 27, 28, 34).Statistical analysis. Changes in cardiovascular variability induced by sympathetic activation with phentolamine were compared with those induced by SNP. Results are expressed as means ± SE. Statistical analysis consisted of Wilcoxon and Mann-Whitney signed rank tests corrected for ties. Significance was assumed at P < 0.05.
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RESULTS |
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METHODS
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DISCUSSION
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Contrasting effects of phentolamine and SNP on cardiovascular
variability.
Both SNP and phentolamine induced reductions in SBP (3 ± 5 from
117 ± 5 mmHg vs. 8 ± 3 from 116 ± 1 mmHg,
respectively) that did not differ significantly (P = 0.26). Changes in DBP also did not differ between SNP (9 ± 5 from 66 ± 4 mmHg) and phentolamine (7 ± 3 from 71 ±3
mmHg, P = 0.53).
130 ± 22 from 972 ± 41 ms) and
MSNA increased (by +184 ± 26%; Table
1 and Fig.
1). As expected, tachycardia and
sympathetic activation were accompanied by increases in normalized LF
variability of RR (+20 ± 6 from 52 ± 5%), MSNA (+3 ± 5 from 36 ± 3%), SBP (+9 ± 6 from 61 ± 6%), and DBP
(+7 ± 5 from 56 ± 4%) (Table
2 and Fig.
2).
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203 ± 31 from 995 ± 42 ms) and greater increases in MSNA (+299 ± 31%) (P < 0.05 for RR and MSNA compared with effects
of SNP; Table 1 and Fig. 1). Despite greater sympathetic activation
with phentolamine, normalized LF cardiovascular variability actually
fell (by 2 ± 7 from 53 ± 6% for RR, by 34 ± 6 from 46 ± 2% for MSNA, by 16 ± 8 from 63 ± 8% for
SBP, and by 13 ± 4 from 54 ± 5% for DBP,
P < 0.05 compared with effects of SNP; Table 2 and
Fig. 2).
Thus both phentolamine and SNP decreased BP. This reduction in BP
resulted in a greater increase in heart rate and MSNA with phentolamine
treatment than with SNP treatment (P < 0.05; Table 1).
However, these hypotensive agents induced opposite changes in the
LF-to-HF ratios of cardiovascular variabilities: the LF-to-HF ratios of
RR, MSNA, and BP decreased with phentolamine (RR 0.7 ± 0.6;
MSNA 0.8 ± 0.2; SBP 3.2 ± 1.4; and DBP 1.4 ± 0.7) and increased with SNP (RR +3.3 ± 1.2, P < 0.01; MSNA +0.2 ± 0.2, P = 0.01, SBP +0.3 ± 1.6, P = 0.09; and DBP +1.5 ± 0.5, P < 0.01 vs. phentolamine, respectively).
Phentolamine slowed the center frequency of the LF components of MSNA
and SBP compared with SNP (P < .05). These
modifications were not due to changes in the center frequency and
variance of respiration (P > 0.87), and phentolamine
did not change the center frequency of the HF components of RR, BP, and
MSNA compared with SNP (P > 0.32).
In all subjects, LF oscillations in RR and BP were evident during
baseline, SNP, and phentolamine sessions (Fig. 2). These LF
oscillations were also present in MSNA during all baseline and SNP
recordings. LF oscillations in MSNA were diminished but still evident
during phentolamine infusion in six subjects (Fig. 2) and disappeared
completely in the other subjects.
Changes in absolute LF and HF spectral powers are shown in Table 2.
Effectiveness of -adrenergic blockade after phentolamine.
The changes in BP, RR, and MSNA induced by phenylephrine alone were
markedly attenuated when phenylephrine was given after administration
of phentolamine (P < 0.05; Figs.
3 and 4).
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DISCUSSION |
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ABSTRACT
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METHODS
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DISCUSSION
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The novel finding of our study is that -adrenergic blockade
eliminates the increased LF variability of sympathetic nerve traffic
that accompanies sympathetic activation in healthy humans. This result
suggests that 1) -adrenergic transmission within the
baroreflex loop is likely to contribute importantly to enhanced LF
oscillatory power associated with sympathetic activation and 2) the rise in LF oscillations during sympathetic activation
may not be exclusively dependent on central mechanisms.
Cardiovascular oscillations slower than those of respiration have been
reported in all mammalian species, but their origin remains unclear.
Respiratory effects on cardiac output produce fluctuations in BP and
subsequently in RR via the baroreflex (2-6, 9, 11,
28). The genesis of the LF oscillations in RR is thought to be
1) a consequence of baroreflex buffering of the HF
oscillations in BP, resulting in a LF 10-s oscillation because of a
resonance phenomenon due to the delay in the sympathetic control loop
of the baroreflex and 2) a baroreflex response to the LF
oscillations in BP (2-6, 9, 11). Thus it is assumed that respiratory BP waves are the afferent signal responsible for the
genesis of LF and HF cardiovascular oscillations. This interpretation
is, however, not unequivocal because there is also clear evidence that
LF cardiovascular oscillations can be generated in the absence of a
functional baroreceptor loop (12, 14, 21, 24, 25, 30), and
a central oscillator in the spinal cord has been hypothesized to be
responsible for LF oscillations in BP in animals, also called Mayer
waves (12, 21, 30). Humans also manifest coherent LF
oscillations between MSNA and BP (28). This finding,
together with the observations that 1) LF oscillations in BP
disappear in the absence of LF oscillations in MSNA (15,
33) and 2) restoration of LF oscillations in MSNA is
also seen in BP (33, 35), suggest that LF oscillations in
MSNA and BP share a common origin. Cyclic release of norepinephrine by
the sympathetic nerve terminals at the neurovascular junction may
contribute to LF oscillations in BP. This hypothesis is further supported by the demonstration that LF oscillations in BP are strongly
attenuated after acute and chronic -adrenergic blockade (8,
19, 20). These studies were performed in animals and did not
record LF variability of sympathetic nerve traffic (8, 19,
20). One of the important findings of the present study is the
demonstration that the reduction in LF variability in BP after
-adrenergic blockade is not due to suppression of vascular responses
to LF oscillations in MSNA because this inhibition of LF oscillatory
power is already present in presynaptic intraneural recordings.
Phentolamine did not completely suppress LF oscillations in BP, RR, or
MSNA in our study. These oscillations tended to become slower than when
sympathetic activation was induced by SNP. This finding is consistent
with studies in animals where -adrenergic blockade did not abolish
LF oscillations in BP (6, 11, 20) and also consistent with
studies in humans where interruption of the baroreflex loop slowed the
LF oscillations during apnea (29). These findings reveal
that LF cardiovascular oscillations may persist even in the absence of
intact neurovascular transmission within the baroreflex in humans.
Neurally independent LF vasomotor oscillations may conceivably be an
autoregulatory property (22, 31). Our observation of
persistent LF oscillations in BP in the absence of LF oscillations in
MSNA in one-third of the subjects also suggests that LF oscillations in
BP may be in part explained by spontaneous fluctuations present in the
vasculature during -adrenergic blockade (3, 22, 31). In
this regard, important information could be drawn by the analysis of
the phase relationships between oscillations in BP and MSNA. However,
this analysis is precluded by the limited number of subjects in whom LF
oscillations in BP were both present and coherent with LF oscillations
in MSNA after phentolamine administration in our study.
Several studies (3-6, 9, 11) have suggested that a resonance phenomenon in the arterial baroreflex loop may contribute to LF cardiovascular oscillations. A time delay in the response of negative feedback systems generates oscillations when the response delay is such that the output becomes in phase with the input, thereby creating a positive feedback (2, 4-6, 9, 11). The frequency of this oscillation depends on the time delay of the response of the system, i.e., the time of signal transmission between the moment when changes in BP sensed by the baroreceptors are translated into changes in vasomotor tone (3-6, 9, 11). This delay is mainly generated by the time needed for norepinephrine secreted at the neuroeffector junction to induce changes in vasomotor tone. With the use of phentolamine, we attenuated the vascular responsiveness to norepinephrine and thereby extended indefinitely the time delay of the baroreceptor feedback. This intervention suppressed the increase in LF cardiovascular variability in response to baroreceptor unloading and sympathetic activation.
Limitations of the study. Our study has several important limitations. First, the sequence of administration of the vasoactive drugs was not randomized due to the long half-life of phentolamine (17). In mitigation, however, performing all recordings during a single session allowed us to compare the sympathetic responses to baroreceptor unloading while maintaining the same microneurographic recording site. Moreover, vasoactive drugs were administered only after the cardiovascular parameters had returned to baseline levels.
Second, phentolamine inhibits both1- and
2-adrenoreceptors (17), and our study
cannot dissociate the contribution of 1- and
2-adrenergic blockade on our results. However, we
verified in each subject that the cardiovascular response to a high
dose of intravenous phenyleprine was markedly blunted after
phentolamine. There is therefore no reason to believe that enhanced
neural release of norepinephrine, due to presynaptic
2-adrenergic blockade, may have overridden
1-adrenergic blockade in our study. We cannot exclude,
however, that other effects of phentolamine, such as reduced
responsiveness to serotonin (17), may have affected our results.
Third, a central effect of phentolamine cannot be ruled out despite
observations that intracisternal phentolamine decreases heart rate
(18) and that the central effects of phentolamine, evident
after an intravenous dose eight times larger than in our study
(16), were not observed at lower doses (13,
26). Our data therefore suggest that -adrenergic transmission
contributes importantly to the increased LF neural and cardiovascular
variability during sympathetic excitation but do not exclude that
central mechanisms participate in generating this LF oscillatory power.
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ACKNOWLEDGEMENTS |
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These studies were supported by a Pfizer Research Grant, by the Foundation for Cardiac Surgery, by the National Fund for Research (to P. van de Borne and J. P. Degaute), and by the Marc Hurard Fondation (to S. Mezzetti). V. K. Somers is an Established Investigator of the American Heart Association and was supported by National Institutes of Health Grants MO1-RR-00585, HL-61560, and HL-65176.
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FOOTNOTES |
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Address for reprint requests and other correspondence: P. van de Borne, Hypertension Clinic, Erasme Hospital, 1070 Brussels, Belgium (E-mail: pvandebo{at}ulb.ac.be).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 11 December 2000; accepted in final form 28 March 2001.
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METHODS
RESULTS
DISCUSSION
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