From the Human Cardiovascular Research Laboratory, Center for Physical
Activity, Disease Prevention, and Aging, Department of Kinesiology, University
of Colorado at Boulder (K.P.D., D.R.S., H.T.), and the Department of Medicine,
Divisions of Cardiology and Geriatric Medicine and Center on Aging, University
of Colorado Health Sciences Center, Denver (D.R.S.), Colo.
Correspondence to Kevin P. Davy, PhD, Department of Exercise and Sport Science, Colorado State University, 212C Moby Complex, Fort Collins, CO 80523. E-mail davy{at}cahs.colostate.edu
Primary aging produces a number of changes in
cardiovascular structure and function in
humans.8 9 It has been proposed that among these
changes is an impairment in cardiopulmonary and integrative
baroreflex sympatho-circulatory control.10 11
This idea is based largely on observations of smaller reflex increases
in FVR in older compared with young adult subjects during both low and
more severe levels of hypovolemia.10 11
In a prior investigation of this issue,12 our
laboratory found that the increases in PNE concentration during graded
hypovolemia were essentially identical in normotensive young and older
adult males but that the increases in FVR tended to be smaller in the
older subjects. In a more recent study,13 we
found similar reflex increases in MSNA in young and older adult men and
women in response to a modest postural challenge (sitting up). Taken
together, our previous observations are more consistent with
the hypothesis that cardiopulmonary and integrative baroreflex
control of SNA is well maintained with advancing age in healthy humans
but that there may be an attenuated peripheral
vasoconstrictor response to sympathetic activation.
Accordingly, in the present study we prospectively tested this
hypothesis. To do so, in a series of experiments we performed direct
(intraneural) recordings of MSNA and determined PNE and FVR in
groups of healthy young and older adult men in the supine position
under control conditions and during progressively greater levels of
hypovolemia induced by graded LBNP.
Experimental Procedures
Experimental Protocols
Protocol 1: MSNA Responses to Graded Hypovolemia
Protocol 2: PVP Responses to Graded Hypovolemia
Protocol 3: FVR Responses to Graded Hypovolemia
Data Analysis
Statistical Analysis
Protocol 1: MSNA Responses to Graded Hypovolemia
Heart rate and arterial blood pressure did not change
significantly from baseline levels during LBNP at -5 to -20
mm Hg in either group (Figures 1
MSNA increased linearly from baseline levels with graded LBNP in both
groups (P<0.05; Figure 1
Protocol 2: PVP Responses to Graded Hypovolemia
Figure 3
Protocol 3: FVR Responses to Graded Hypovolemia
The FBF and FVR responses to progressive hypovolemia are illustrated in
Figure 4
The relation between the mean increases in FVR and MSNA during graded
hypovolemia is shown in Figure 5
For all comparisons, the same age group–related differences were
obtained when decreases in forearm vascular conductance were used to
express the limb vasoconstrictor responses to LBNP as when increases in
FVR were used.
There are 2 primary new findings from the present investigation
related to our working hypothesis. First, it appears that
cardiopulmonary and integrative (ie, combined
cardiopulmonary and arterial) baroreflex control of
MSNA during hypovolemia is augmented, rather than impaired, with
advancing age in healthy adult humans. Second, the smaller increase in
FVR during hypovolemia-induced baroreflex deactivation reported
previously in older adults10 11 likely is due to
an attenuated vasoconstrictor response to sympathetic stimulation.
Based largely on observations of smaller increases in FVR in response
to graded hypovolemia in older compared with young adults, it has been
concluded that cardiopulmonary and integrative baroreflex
sympatho-circulatory control becomes impaired with advancing age in
humans.10 11 The present findings (Figure 4
The present results are consistent with our previous
observations of similar increases in PNE concentration but a tendency
for smaller increases in FVR in older compared with young adult males
during graded hypovolemia.12 Our findings also
agree with recent studies in humans reporting attenuated FVR responses
to norepinephrine infusion19 and
delayed pressor responses to breathing-induced increases in
MSNA20 in older adult humans. An age-related
decline in
In our earlier related investigations,12 13 we
found that arterial blood pressure was regulated as well or
better in healthy normotensive older humans compared with young adult
controls during acute hypovolemia. The present study confirms these
prior observations. Specifically, arterial blood pressure
was well maintained in both age groups during low-moderate levels of
LBNP (Figure 2
Precise regulation of arterial pressure in the face of an
attenuated peripheral vasoconstriction in the older
subjects deserves comment. The most likely explanation is that stroke
volume and cardiac output declined less during the more severe levels
of hypovolemia, as we observed in our previous
study,12 due in part to age-related increases in
ventricular and vascular stiffness.10
In this context, Cleroux and colleagues10 found
that the reduction in central venous pressure during -40 mm Hg
LBNP was associated with less of a decline in left
ventricular end-diastolic volume (and
presumably stroke volume) in older compared with young adult humans.
This might result in less translocation of central blood volume to the
periphery22 and therefore a smaller challenge to
arterial blood pressure control in the older males. Another
possibility is that greater vasoconstriction was evoked in other (ie,
nonskeletal muscle) regional circulations in the older subjects than in
the young adult controls.
A smaller challenge to arterial blood pressure
maintenance may also explain the smaller heart rate response to
the higher levels of LBNP in this (Figure 1
The greater reflex increase in MSNA during graded hypovolemia in the
older subjects (Figure 3
There are at least 4 important caveats associated with the present
study that should be mentioned. First, the results of recent studies in
humans suggest that changes in aortic26 and
carotid27 28 artery dimensions are observed even
during low levels of LBNP, suggesting that arterial as well
as cardiopulmonary baroreflexes may be deactivated
throughout graded hypovolemia. Therefore, the specific baroreflexes
that were unloaded under these conditions, and thus contributed to the
stimulation of MSNA, cannot be determined with certainty. Because there
is no reflex tachycardia suggestive of robust
arterial baroreflex involvement during low levels of LBNP,
however, it is likely that cardiopulmonary baroreflexes play a
major role in the regulation of MSNA during mild hypovolemia in humans.
With increasing levels of hypovolemia that produce a progressively
greater challenge to arterial blood pressure
maintenance, arterial baroreflex deactivation
presumably contributes in an increasingly greater manner to the
stimulation of MSNA. In the present study, we found that
Second, we measured SNA in the lower leg and blood flow in the forearm
in the present study. However, Rea et al29
have established that graded LBNP elicits similar increases in MSNA in
the leg and arm in humans.
Third, it is possible that the attenuated limb vasoconstrictor response
to sympathetic stimulation in the older subjects was due in part to a
smaller rate of release from sympathetic nerve endings and consequent
lower synaptic concentration of norepinephrine (ie, rather
than reduced vasomotor responsiveness to norepinephrine).
Without more direct measures of PNE kinetics from the forearm, we
cannot determine the likelihood of this possibility. However, the facts
that (1) PNE concentrations obtained from antecubital venous blood
samples were similar in the 2 groups and (2) PNE clearance, including
the reuptake 1 mechanism, decreases with age in
humans30 (which would act to elevate rather than
reduce synaptic concentrations) are inconsistent with this
idea. Moreover, the limited available data suggest that sympathetic
innervation of skeletal muscle arterioles is not related to age in
healthy adult humans.31
Finally, because our interest in gerontology and geriatric medicine
centers on the role of primary aging in cardiovascular
health and disease, we studied older subjects who were normotensive and
otherwise free of overt cardiovascular disorders. In
this context, we should emphasize that less healthy older adults may
demonstrate impaired baroreflex control of SNA secondary to the effects
of hypertension and/or other forms of cardiovascular
disease.
In conclusion, the present findings provide experimental support
for the concept that cardiopulmonary and integrative baroreflex
control of SNA during acute hypovolemia is enhanced rather than
depressed in healthy older humans. This may help minimize the
functional impact of a marked age-related reduction in
peripheral vasoconstrictor responsiveness to sympathetic
neural stimulation and contribute to the effective regulation of
arterial blood pressure in older adults during
orthostatic challenge.
Received January 21, 1998;
first decision February 6, 1998;
accepted March 11, 1998.
© 1998 American Heart Association, Inc.
Scientific Contributions
Augmented Cardiopulmonary and Integrative Sympathetic Baroreflexes but Attenuated Peripheral Vasoconstriction With Age
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Abstract—Based on observations of
smaller increases in limb vascular resistance during acute incremental
hypovolemia in older adults, cardiopulmonary and integrative
(combined cardiopulmonary and arterial) baroreflex
control of sympatho-circulatory function is thought to be impaired with
aging in humans. We tested this hypothesis directly by making
intraneural measurements of skeletal muscle sympathetic nerve activity
(MSNA; peroneal microneurography) in groups of young (23±1 years;
n=11) and older (64±1 years; n=12) healthy adult men during
progressive hypovolemia produced by graded (-5 to -40 mm Hg)
lower body negative pressure (LBNP). Baseline levels of MSNA and
arterial blood pressure were higher and heart rate was
lower in the older subjects (P<0.05). Lower levels of
LBNP (-5 to -20 mm Hg) did not affect arterial
blood pressure or heart rate in either group; systolic and
pulse pressures declined during higher levels of LBNP (-30 and
-40 mm Hg) but only in the young subjects
(P<0.05). Graded LBNP evoked progressive, linear
reductions in peripheral venous pressure (PVP) and
increases in MSNA, plasma norepinephrine concentration
(PNE), and forearm vascular resistance (FVR) in both groups (all
P<0.05). 
MSNA/PVP was 
150% greater in the
older versus young men during both lower and higher levels of
hypovolemia (P<0.01); however, FVR/PVP was
50% smaller in the older men (P<0.05). There was no
difference in the MSNA-PNE relation with age, but FVR/MSNA was
65% to 70% smaller in the older subjects (P<0.05).
Our findings indicate that cardiopulmonary and integrative
baroreflex control of central sympathetic outflow during hypovolemia is
augmented, not impaired, with age in healthy humans. However, the
reflex-mediated increases in limb vascular resistance during
hypovolemia are smaller in older adults because of attenuated
vasoconstrictor responsiveness to sympathetic stimulation.
Key Words: hypovolemia • aging • blood pressure
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
The
cardiopulmonary and arterial baroreflexes play a
critical role in maintaining circulatory homeostasis, in large part
through their tonic inhibition of SNA.1 2 In
humans, baroreflex control of SNA often has been studied using graded
hypovolemia.1 2 Low levels of hypovolemia at
which heart rate and arterial blood pressure are unaffected
are thought to preferentially deactivate
cardiopulmonary baroreflexes and evoke increases in skeletal
MSNA, PNE concentration, and limb vascular
resistance.1 2 3 4 5 6 7 More severe levels of hypovolemia
that cause tachycardia and, at least in healthy young
adults, reductions in arterial blood pressure are thought
to unload both cardiopulmonary and arterial
baroreceptors, resulting in a greater and more systemic
"integrative" baroreflex stimulation of
SNA.1 2 4 5
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Subjects
Eleven young and 12 older healthy nonobese men participated in
the present investigation. All subjects were normotensive and free
from overt cardiovascular disease, as assessed from
casual blood pressure measurements and medical history. Older subjects
were further evaluated for clinical evidence of cardiopulmonary
disease with a physical examination and resting and maximal exercise
ECG. All subjects were nonsmokers, and none took medications that could
affect autonomic-circulatory function. The nature, purpose, and risks
of the study were explained to each subject before written informed
consent was obtained. The study was approved by the Human Research
Committee at the University of Colorado.
Multiunit recordings of MSNA were obtained from the
right peroneal nerve using the microneurographic technique as
previously described.13 14 15 16 The neural activity
was amplified, filtered (700 to 200 Hz), full-wave rectified, and
integrated (time constant, 0.1 second). Recordings of efferent
MSNA were deemed acceptable according to previously described
criteria.16 Heart rate was obtained from an ECG,
and beat-to-beat arterial pressure was measured
continuously using the finger photoplethysmographic technique (Finapres
model 2300, Ohmeda).12 PVP (Statham model P23,
Gould Instruments) was measured using the method of Gauer and
Sieker17 as described previously by our
laboratory.12 Under these conditions, changes in
PVP recorded from a catheter placed in a large antecubital vein of
the dependent arm accurately reflect changes in central venous pressure
(r=0.96).17 Whole FBF was measured in
the right arm using venous occlusion plethysmography as previously
described.12 Respiratory excursions were measured
with a pneumobelt placed around the upper abdomen. PNE concentration
was determined using the single-isotope radioenzymatic technique of
Peuler and Johnson18 as described
previously.14
All experimental protocols were performed in the morning after a
12-hour overnight fast with proper hydration. Subjects were sealed at
the level of the iliac crests in a chamber designed for administering
LBNP; this was standardized across all 3 experimental protocols. Stable
control levels of all variables were obtained for at least 10
minutes before the initiation of suction. LBNP was administered during
consecutive 5-minute periods at each of the following levels: -5,
-10, -15, -20, -30, and -40 mm Hg. Subjects underwent the
following experimental protocols on separate days.
MSNA, heart rate, and arterial blood pressure were
measured continuously during baseline control and LBNP with subjects in
a supine position (Table
). Venous blood
samples for subsequent determination of PNE concentration were obtained
during the last minute of the control period and through the -20
mm Hg level of LBNP. Problems with blood sampling were encountered in
several subjects at -30 and -40 mm Hg LBNP; thus, data for PNE
are reported only for the initial 4 levels of hypovolemia. Eleven young
and 12 older subjects initiated this protocol. Because of presyncopal
symptoms or nonspecific discomfort, the number of subjects completing
various levels of LBNP were 9 young and 11 older men through -20
mm Hg; 8 young and 9 older men through -30 mm Hg; and 7 young
and 9 older men through -40 mm Hg.
View this table:
[in a new window]
Table 1. Subject Characteristics and Baseline Levels of
Arterial Blood Pressure, Heart Rate, and MSNA
PVP (measure of the hypovolemic stimulus), heart rate, and
arterial blood pressure were measured continuously during
baseline control and LBNP. Subjects were in the right lateral decubitus
position with the right arm extended downward as described
previously.12 17 The numbers of subjects
completing the various levels of LBNP in this protocol and protocol 3
below were similar to those described above for protocol 1.
FBF, heart rate, and arterial blood pressure were
measured during baseline control and LBNP with subjects in the supine
position. FVR was calculated from mean arterial blood
pressure/FBF.
MSNA, heart rate, and arterial blood pressure were
recorded continuously on a Gould ES1000 recorder (Gould
Instruments) and were stored on videocassette (A.R. Vetter) for
subsequent computer analysis. PVP and FBF were calculated
manually from chart recorder tracings. The bursts of MSNA, PVP
waves, and FBF curves were measured by the same investigator (H.T.),
who was blinded to the identity of the subjects. MSNA was expressed as
total minute activity (arbitrary units) and quantified by computer
measurements of area under each burst of neural
activity.15 The forearm vasoconstrictor responses
to LBNP also were analyzed as changes in vascular conductance
(ie, FBF/mean arterial blood pressure).
A one-way ANOVA was used to test for differences in each subject
characteristic. Main effects for group and time for each dependent
variable were assessed by repeated-measures ANOVA. A Newman-Keuls
post hoc procedure was used to test for differences between groups at a
particular time point or within groups across time. Simple linear
regression and univariate correlational analyses
were used to determine the relations between MSNA and PVP and between
MSNA and FVR in the young and older men. ANCOVA was used as a
complementary approach to the ratio method for examining possible group
differences in the MSNA/PVP and the FVR/MSNA responses to
LBNP. The significance level was set at P<0.05. All values
are presented as mean±SE.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Subject Characteristics
The older men were 40 years older than the young adult controls
(64±1 versus 23±1 years; P<0.05). However, the 2 groups
did not differ significantly in height (176±2 versus 179±2 cm), body
mass (77.1±2.2 versus 76.7±2.0 kg), or body mass index (25.0±0.6
versus 23.9±0.6). Although well within the normotensive range, resting
brachial systolic arterial blood pressure was
higher in the older (124±3 mm Hg) compared with the younger
(113±4 mm Hg) men (P<0.05); there were no group
differences in resting brachial diastolic
arterial blood pressure (76±2 versus 73±3, older versus
younger).
Baseline heart rate was lower (Figure 1) and Finapres-measured systolic
and mean arterial blood pressures were higher (Figure 2) in the older subjects. MSNA burst
frequency (42±3 versus 21±2 bursts per minute) and total activity
(Figure 1) were higher in the older men during supine rest
(P<0.05), but PNE concentration (Figure 1) did not differ
with age.
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[in a new window]
Figure 1. Sympathetic and cardiovascular
responses to graded hypovolemia in young and older healthy adult men.
Values are mean±SE. *P<0.05 vs young subjects.
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Figure 2. Arterial blood pressure (BP) during
graded hypovolemia in young and older healthy adult men. Values are
mean±SE. *P<0.05 vs young subjects. 
and 2). In the young controls, LBNP
at -30 and -40 mm Hg elicited reductions in systolic
and pulse pressures but no significant changes in diastolic
or mean pressures. In contrast, the older men demonstrated unchanged
systolic and pulse pressures but increased
diastolic and mean pressures during these higher levels of
LBNP. Heart rate increased above baseline levels in both groups during
-30 and -40 mm Hg of LBNP (P<0.05); the magnitudes
of the increases were smaller in the older men
(P<0.05). ). The older men tended to
demonstrate greater increases in MSNA compared with the young adult
controls (P=0.06). PNE concentration increased linearly from
baseline levels during graded LBNP (P<0.05), with no group
differences in the magnitudes of the increases (Figure 1). The relation
between PNE concentration and MSNA during progressive hypovolemia did
not differ with age (P>0.3).
The arterial blood pressure and heart rate responses
to graded hypovolemia were not different during this protocol compared
with those observed in protocol 1. Baseline PVP was not different in
the young and older subjects (Figure 1). PVP decreased linearly
throughout LBNP in both groups (P<0.01; Figure 1); the
reductions tended to be smaller in the older men, but the differences
were not statistically significant (P=0.15). illustrates the mean increases
in MSNA per millimeter of mercury mean reduction in PVP
(MSNA/PVP) during graded hypovolemia in the young and older men.
The slope of the line was greater in the older subjects
(P<0.05). The corresponding mean MSNA/PVP was
150% greater in the older men than in the young adult controls
during the lower (-5 through -20 mm Hg LBNP), the higher (-30
and -40 mm Hg LBNP), and the overall (-5 through -40
mm Hg LBNP) levels of hypovolemia (P<0.05). ANCOVA with
PVP as the covariate confirmed that the MSNA response to graded
hypovolemia was greater (P<0.05) in the older subjects.
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Figure 3. Relation between changes in MSNA and PVP during
graded hypovolemia in young and older healthy adult men. Insert shows
mean age group differences in MSNA/PVP during the lower and
higher levels of LBNP, respectively. Values are mean±SE.
*P<0.05 vs young subjects.
The arterial blood pressure and heart rate responses
to graded hypovolemia were not different during this protocol compared
with those observed in protocols 1 and 2. Supine resting baseline
levels of FBF and FVR (Figure 4) and
forearm vascular conductance (0.038±0.005 versus 0.038±0.006 U) were
not significantly different in the young and older men.
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Figure 4. FBF and FVR during graded hypovolemia in young and
older healthy adult men. Values are mean±SE. *P<0.05
vs young subjects. . FBF decreased and FVR increased with graded LBNP in both
groups (P<0.05). The reductions in FBF were not
significantly different in the 2 groups but tended to be smaller in the
older men. However, the increases in FVR were smaller in the older men
for the 
-10 mm Hg levels of LBNP (P<0.05 to
P<0.01). Moreover, mean FVR/PVP was 50% smaller
in the older men compared with the young adult subjects during the
lower (1.9±0.6 versus 3.9±0.6), the higher (2.5±0.5 versus
5.1±0.7), and the overall (1.9±0.4 versus 4.1±0.6) levels of
hypovolemia (all P<0.05). . The
slope of the line was smaller in the older subjects
(P<0.05). The mean FVR/MSNA was 65% to 70%
smaller in the older than in the young adult subjects during the lower
(0.007±0.005 versus 0.024±0.005), the higher (0.006±0.005 versus
0.019±0.003), and the overall (0.007±0.005 versus 0.020±0.004)
levels of hypovolemia (all P<0.05). ANCOVA with MSNA as the
covariate confirmed that the FVR response to graded hypovolemia was
attenuated in the older subjects (P<0.05).
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Figure 5. Relation between changes in FVR and MSNA during
graded hypovolemia in the young and older healthy adult men. Insert
shows mean age group differences in FVR/MSNA during the lower and
higher levels of LBNP, respectively. Values are mean±SE.
*P<0.05 vs young subjects.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
To our knowledge, this is the first investigation of the effects
of aging on cardiopulmonary and integrative baroreflex
regulation of directly measured SNA in humans. Moreover, this is the
first study in humans to determine age-related changes in the relation
between SNA and peripheral vasoconstrictor
responsiveness. )
confirm these previous observations of an age-related attenuation in
the FVR response to hypovolemia. Our results (Figure 5), however,
demonstrate that this likely is the result of nonneural changes
affecting vasoconstrictor responsiveness rather than an impairment in
baroreflex control of SNA. In fact, the latter actually appears to be
enhanced in healthy older adults (Figure 3). This apparent augmented
sympathetic baroreflex sensitivity may have functional importance in
acting to counter the apparent age-related reduction in vascular
responsiveness to sympathetic neural activation. 
-adrenergic vasoconstriction in response to
norepinephrine and nerve stimulation also has been reported
in human subcutaneous arteries studied in
vitro.21 The smaller age-related increases in FVR
in response to graded hypovolemia in the present study likely
represent attenuated skeletal muscle vasoconstrictor
responsiveness, since we have previously shown that skin vascular
resistance is not altered in young and older adult males during this
stimulus.12 ). At the 2 highest levels of LBNP (-30 and -40
mm Hg), however, systolic and pulse pressures fell
significantly below baseline levels in the young but not in the older
men. ) and our
previous12 studies. That is, less of an
arterial baroreflex-mediated tachycardia would
be required to maintain arterial pressure under these
circumstances. The lack of decline in arterial
systolic and pulse pressures in the older males during these
higher levels of LBNP in the present investigation suggests that
the arterial baroreceptors may not have been unloaded to
the same extent as that observed in the young controls. Thus, the
absence of a robust tachycardia in the older subjects
should not necessarily be interpreted as evidence for impaired
arterial baroreflex control of heart rate with aging. ) was observed despite at least 2 potentially
counteracting factors. The first is the possible lesser degree of
arterial baroreceptor unloading at the higher levels of
LBNP, as discussed above. The lack of any fall in arterial
pressure in the older men should represent less of a stimulus
for reflex sympathetic activation, yet an augmented response was
demonstrated. Second, the greater reflex increases in MSNA in the older
subjects were observed despite their higher baseline levels.
We14 and others4 23 24
previously have established that resting levels of MSNA increase
markedly with age, even in healthy men and women. In an earlier report,
Iwase and colleagues24 suggested that such high
baseline levels of MSNA limited the ability of older humans to evoke
increases in MSNA during orthostatic stress. However, both
the present results (Figures 1 and 3) and our previous studies on
upright sitting and other forms of laboratory
stress13 15 demonstrate that older adults evoke
as great or greater absolute increases in MSNA in response to
sympatho-excitatory stimuli as young adults. Moreover, the present
results are consistent with recent findings that integrative
baroreflex-mediated increases in MSNA in response to
intravenous administration of vasodilator drugs (which
produce changes in both systemic arterial and central
venous pressures) are not impaired in middle-aged and older humans
despite their elevated resting levels of
MSNA.23 25 MSNA/PVP was 150% greater in the older subjects during both
the lower and higher levels of hypovolemia. As such, our results are
consistent with the concept that both the
cardiopulmonary and the integrative (cardiopulmonary
and arterial) sympathetic baroreflexes may have been more
sensitive in the older men.
Selected Abbreviations and Acronyms
FBF
=
forearm blood flow
FVR
=
forearm vascular resistance
LBNP
=
lower body negative pressure
MSNA
=
muscle sympathetic nerve activity
PNE
=
plasma norepinephrine
PVP
=
peripheral venous pressure
SNA
=
sympathetic nerve activity
Acknowledgments
This study was supported by National Institutes of Health RO1
awards AG06537, AG13038, and HL39966 (Dr Seals); NIH KO1 award AG00687
(Dr Davy); and NIH F32 awards HL08834 (Dr Davy) and AG05717 (Dr
Tanaka). We would like to acknowledge the technical assistance of Mary
Jo Reiling.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
-adrenergic responsiveness is decreased and SNS activity is
increased in older humans. Am J Physiol. 1994;266:E717–E724.-adrenoceptor-mediated
contractility of isolated human resistance arteries.
Am J Physiol. 1992;263:H1190–H1196.
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 A. Sakima, D. B. Averill, P. E. Gallagher, S. O. Kasper, E. N. Tommasi, C. M. Ferrario, and D. I. Diz Impaired Heart Rate Baroreflex in Older Rats: Role of Endogenous Angiotensin-(1-7) at the Nucleus Tractus Solitarii Hypertension, August 1, 2005; 46(2): 333 - 340. [Abstract] [Full Text] [PDF]
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F. C. de Carvalho, F. M. Consolim-Colombo, C. A. Pastore, M. C. Rubira, J. C. Meneguetti, E. M. Krieger, and M. Wajngarten Acute reduction of ventricular volume decreases QT interval dispersion in elderly subjects with and without heart failure Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2171 - H2176. [Abstract] [Full Text] [PDF]
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P. J Fadel, Z. Wang, H. Watanabe, D. Arbique, W. Vongpatanasin, and G. D Thomas Augmented sympathetic vasoconstriction in exercising forearms of postmenopausal women is reversed by oestrogen therapy J. Physiol., December 15, 2004; 561(3): 893 - 901. [Abstract] [Full Text] [PDF]
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D. R. Seals and F. A. Dinenno Collateral damage: cardiovascular consequences of chronic sympathetic activation with human aging Am J Physiol Heart Circ Physiol, November 1, 2004; 287(5): H1895 - H1905. [Abstract] [Full Text] [PDF]
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 J. P. Hernandez and W. D. Franke Age- and fitness-related differences in limb venous compliance do not affect tolerance to maximal lower body negative pressure in men and women J Appl Physiol, September 1, 2004; 97(3): 925 - 929. [Abstract] [Full Text] [PDF]
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Q. Fu, A. Arbab-Zadeh, M. A. Perhonen, R. Zhang, J. H. Zuckerman, and B. D. Levine Hemodynamics of orthostatic intolerance: implications for gender differences Am J Physiol Heart Circ Physiol, January 1, 2004; 286(1): H449 - H457. [Abstract] [Full Text] [PDF]
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A. U. Ferrari, A. Radaelli, and M. Centola Invited Review: Aging and the cardiovascular system J Appl Physiol, December 1, 2003; 95(6): 2591 - 2597. [Abstract] [Full Text] [PDF]
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D. N. Proctor, S. C. Newcomer, D. W. Koch, K. U. Le, D. A. MacLean, and U. A. Leuenberger Leg blood flow during submaximal cycle ergometry is not reduced in healthy older normally active men J Appl Physiol, May 1, 2003; 94(5): 1859 - 1869. [Abstract] [Full Text] [PDF]
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 P. P. Jones, D. D. Christou, J. Jordan, and D. R. Seals Baroreflex Buffering Is Reduced With Age in Healthy Men Circulation, April 8, 2003; 107(13): 1770 - 1774. [Abstract] [Full Text] [PDF]
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G. E. Alvarez, S. D. Beske, T. P. Ballard, and K. P. Davy Sympathetic Neural Activation in Visceral Obesity Circulation, November 12, 2002; 106(20): 2533 - 2536. [Abstract] [Full Text] [PDF]
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K. D. Monahan and C. A. Ray Vestibulosympathetic reflex during orthostatic challenge in aging humans Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2002; 283(5): R1027 - R1032. [Abstract] [Full Text] [PDF]
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F. A. Dinenno, N. M. Dietz, and M. J. Joyner Aging and Forearm Postjunctional {alpha}-Adrenergic Vasoconstriction in Healthy Men Circulation, September 10, 2002; 106(11): 1349 - 1354. [Abstract] [Full Text] [PDF]
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M. S. Olufsen, A. Nadim, and L. A. Lipsitz Dynamics of cerebral blood flow regulation explained using a lumped parameter model Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2002; 282(2): R611 - R622. [Abstract] [Full Text] [PDF]
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P. P. Jones, L. F. Shapiro, G. A. Keisling, J. Jordan, J. R. Shannon, R. A. Quaife, and D. R. Seals Altered Autonomic Support of Arterial Blood Pressure With Age in Healthy Men Circulation, November 13, 2001; 104(20): 2424 - 2429. [Abstract] [Full Text] [PDF]
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