Vol. 275, Issue 2, H409-H415, August 1998
Arterial response during cold pressor test in borderline
hypertension
A. B.
Lafleche1,
B. M.
Pannier2,
B.
Laloux1, and
M. E.
Safar1
1 Department of Internal
Medicine and Institut National de la Santé et de la Recherche
Médicale (U337), Broussais Hospital, 75014 Paris, and
2 Manhès Hospital,
Fleury-Merogis 91700, France
 |
ABSTRACT |
We observed previously that sympathetic
activation produced by lower body negative pressure increases
pulse-pressure amplification with little change in mean pressure.
Whether the cold pressor test (CPT) might produce a similar hemodynamic
pattern has been ignored. Ten subjects with borderline hypertension and
ten age- and sex-matched normotensive controls were compared to
investigate carotid-brachial pulse-pressure amplification (aplanation
tonometry) and changes in brachial and carotid distensibility
(echotracking technique) before and during CPT. The maneuver markedly
increased blood pressure without a change in heart rate. Pulse-pressure amplification tended to disappear as a consequence of a higher increase
in carotid than in brachial pulse pressure, due to an earlier return of
wave reflections at the carotid site. CPT caused a significant decrease
in carotid and brachial distensibility. Both results were more
pronounced in controls than in borderline hypertensives. Thus CPT
reduces pulse-pressure amplification. In humans, this change may
greatly influence the calculation of arterial distensibility, although
this point is usually minimized in animal experiments. Furthermore, in
young subjects, sympathetic stimulus may induce different arterial
responses, depending on the mechanism involved: reflex or global
nonspecific stimulus.
pulsatile arterial hemodynamics; wave reflection
| |
INTRODUCTION |
THE BLOOD PRESSURE CURVE may be divided into two
components: a steady component, mean arterial pressure, and a pulsatile
component, pulse pressure, which is the difference between peak
systolic and end-diastolic blood pressure (29). Whereas
mean arterial pressure remains almost constant along the arterial tree,
pulse pressure increases markedly from central to peripheral arteries (15, 29). This is due to the changing pattern in the timing of wave
reflections when the blood pressure propagates along arterial conduits
with a progressive decrease in lumen diameter and an increase in
vascular rigidity. We have previously shown (31) that the activation of
the autonomic nervous system produced by lower body negative pressure
(LBNP) is able not only to cause a slight decrease in mean arterial
pressure and a significant increase in heart rate but also to enhance
pulse-pressure amplification as a consequence of a substantial decrease
in central (carotid) pulse pressure with minimal changes in peripheral
(brachial) pulse pressure. However, whether other maneuvers that
activate the sympathetic nervous system may cause similar changes in
pulse-pressure amplification has never been investigated.
The cold pressor test (CPT) is known to cause a global sympathetic
activation in subjects with different levels of baseline sympathetic
tone, such as a group of normal subjects and patients with borderline
hypertension (23, 36). CPT results in a significant arteriolar
vasoconstriction, with a subsequent increase in blood pressure and a
slight increase in plasma catecholamines but with no change in heart
rate (1, 5, 8, 32, 37). Associated changes in the rigidity of large
arterial vessels have been observed (10), but, in normal volunteers,
major discrepancies have been noted at the site of the radial artery
(3, 12). In particular, decreased or increased values of distensibility
and compliance have been obtained depending on the intensity of the
stimulus and the number of pulse-pressure measurements. Because
distensibility is the ratio between pulsatile diameter and pulsatile
pressure, it is important to determine whether the sympathetic
activation produced by CPT is able to substantially modify pulse
pressure and greatly modify pulse-pressure amplification.
In the present report, we investigated a population of subjects with
borderline hypertension in comparison with a group of age- and
sex-matched normotensive controls. The goal of the study was twofold:
1) to evaluate whether
pulse-pressure amplification is modified by CPT, and
2) to determine the changes in
arterial diameter and distensibility at the site of two different
arteries, a peripheral, medium-sized muscular artery, the brachial
artery, and a central elastic artery, the common carotid artery (9). In
both cases, distensibility was measured from local pulse pressure and
pulsatile diameter using a high-resolution echotracking technique.
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METHODS |
Patients.
Ten Caucasian borderline hypertensive patients (8 males, 2 females)
ages 21-58 yr (33 ± 13 yr, mean ± SD) and 10 normotensive subjects (7 males and 3 females) ages 28-45 yr (35 ± 6 yr)
were studied in the morning after they had consumed a light,
standardized breakfast in a temperature-controlled room (22 ± 2°C). Normotension was defined as auscultatory blood pressure
<140/90 mmHg measured at three different times over a 2-wk period.
Borderline hypertension (BHT) was defined as two casual blood pressure
recordings with a diastolic blood pressure (DBP) 
90 mmHg during the
previous 12 mo, plus at least two measurements with a DBP <90 mmHg
(34). No patients had cardiovascular complication or other
diseases. None of them had been previously treated with cardiovascular
agents. The principal clinical characteristics of the subjects are
given in Table 1. All of them gave informed
consent, and the study was approved by the Ethical Committee of
Broussais Hospital.
Description of study and CPT.
Baseline conditions were recorded after 20 min of rest in the supine
position. Investigations included brachial automatic blood pressure
measurement every 2 min with a Dinamap apparatus (Critikon,
Chatenay-Malabry, France) on the left arm (homolateral to the cold
pressor stimulus), measurement of the right common carotid artery
geometry with an echotracking system, followed by measurement of the
right carotid artery local pulse pressure (PP) with the aplanation
tonometry method, and then, using the same methods, recordings of
geometry and PP at the right brachial artery at the level of the elbow,
with the upper limb maintained in an armrest.
The CPT was performed by immersing the left hand up to the wrist in
ice-cold water at 4°C for 5 min (37). All measurements were begun
after 30 s of stimulus. Dinamap blood pressure recordings were made
every minute. Only one recording of geometric and pressure measurements
was made at both arterial sites by two trained investigators simultaneously during the 5 min of stimulus, but all the arterial measurements were finished at the beginning of the 5th minute of
Dinamap blood pressure recording.
PP and central arterial reflection wave measurement.
The carotid and radial PP were measured with a transcutaneous
aplanation tonometry system (Millar, Houston, TX) (13, 21, 22).
Briefly, the carotid PP wave is recorded with a high-fidelity strain-gauge transducer internally calibrated (1 mV = 1 mmHg) with a preamplifier on a paper recorder at the speed of 100 mm/s (Siemens, Saint Denis, France). The probe is handheld and
positioned at the level of the artery where the signal is the best and
most accurate in terms of shape and amplitude. The use of this method requires training to obtain accurate and adequate angulation between the probe and the vessel axis, because transducer movements caused by
movements of the patient or the operator's hand or by inappropriate hold-down pressure can alter the quality of the recording, as described
by Kelly et al. (13). Validation of PP determination using simultaneous
intra-arterial measurements has been previously published in detail (1,
7).
This method also allows the analysis of the timing of wave reflections
by using the changes in the shape of the pressure curve at the level of
the carotid artery and ascending aorta during the cardiac cycle
(7). The aortic PP waveform has been extensively described
already and was generally shown as manifesting an inflection point
(Pi) dividing the pressure wave
into an early and a mid-to-late systolic peak (7, 16, 19, 22, 31). This
inflection point has been described as indicating two different
waveform components on the recorded pressure: a forward, or incident,
wave and a backward, or reflected, wave. The mid-to-late systolic peak is interpreted as the result of the reflected wave coming back from
peripheral sites of reflection and is responsible for a late increase
in PP and systolic blood pressure (SBP). The maximal peak
(Pk) of the blood pressure curve
is influenced by the timing and the amplitude of this reflected wave.
When the reflected wave is attenuated and/or delayed, this wave
will not contribute to the maximal aortic systolic peak:
Pk will happen early in systole, Pi will appear after
Pk, and
(Pk 
Pi) will be expressed
conventionally as a negative value. In that case,
(Pk Pi) is only an indicator of the
contribution of the reflected wave to the late systolic pressure. In
younger subjects, Pi may be
particularly difficult to evaluate during systole because the reflected
wave occurs during diastole after the aortic valve closure. When the
backward pressure is not attenuated and/or delayed, the
reflected wave will contribute to the aortic peak SBP:
Pk will happen later than
Pi, and
(Pk Pi) will be expressed as a
positive value, thus representing the amplification of PP and SBP due
to the reflected wave. Finally, the ratio of
(Pk Pi) to PP (as a percentage),
expressed conventionally as a negative or a positive value, is
considered a rough indicator of the relative contribution of the
reflected pressure wave to the systolic pressure in central arteries,
particularly the ascending aorta. On the other hand, the delay from the
foot of the pressure wave to the
Pi
(Dtp) has been interpreted as
representing the travel time for the incident wave to reach the
peripheral reflecting sites and return (16, 28). Left ventricular
ejection time (LVET) was measured from the foot of the pressure wave to
the diastolic incisura. Murgo et al. (28) classified the aortic pressure waveform, depending on age and hypertensive status, into three
subgroups according to its shape: type A, in which
Pk occurs in late systole after a
well-defined Pi and
(Pk Pi)/PP > 0.12; type C, in
which Pk precedes
Pi and
(Pk Pi)/PP < 0.0; and type B,
which is the same as type A except that 0.0 < (Pk Pi)/PP < 0.12. Typically, type
A is observed in older subjects and hypertensive patients, and type C
is observed in normotensive subjects and younger subjects. SBP and PP
may increase significantly from central to peripheral arteries. This
contrasts with drops in DBP and mean blood pressure (MBP) from the
ascending aorta to the radial artery that do not exceed 1-2 mmHg
(15, 29). Therefore, carotid SBP and PP were estimated from the carotid
pressure waveform, with the assumption that brachial and carotid DBP
and MBP were equal, with the use of the HP Sketch Pro Tablet Digitizer
connected to a PC. Carotid MBP was computed from a carotid pressure
tracing from the area of the carotid pressure waveform, determined from the Tablet Digitizer, and was set equal to brachial MBP (21). Repeatability of measurements has been previously reported (31).
Pulsatile changes in arterial diameter measurement.
The artery diastolic diameter
(Dd) and its
absolute and relative changes during the systolic-diastolic periods
[systolic diameter (Ds) Dd and
(Ds Dd)/Dd]
were measured with a high-fidelity vascular echotracking system (WTS,
Maastricht, The Netherlands) (11, 14). Briefly, this apparatus enabled
us to assess transcutaneously the displacement of the arterial walls
during the cardiac cycle and, hence, the time-dependent changes in
arterial diameter relative to its initial diameter at the beginning of
the cardiac cycle. On the basis of the two-dimensional B-mode image, an
M-line was selected perpendicular to the artery, the radiofrequency
echographic signal of four to eight cardiac cycles was recorded
digitally, and a tracking system allowed the vessel walls to be tracked
during the whole cardiac cycles.
Dd,
(Ds Dd), and
(Ds Dd)/Dd
were automatically calculated in a few seconds by the computer.
From these geometric and pressure variables, the distensibility
coefficient (DC) and cross-sectional compliance (CSC) were calculated.
CSC is equal to
[(Ds Dd)/2PP]
Dd,
and DC is
[2(Ds Dd)/Dd]/PP
(4, 17, 31, 35). Repeatability of measurements has been described in
detail elsewhere (31).
Statistical analysis.
Results are expressed as means ± SD. The clinical characteristics
of both groups were compared with the use of a
t-test for unpaired values (NCSS
software, Kaysville, UT). We analyzed the changes in blood pressure and
heart rate minute by minute throughout the CPT using a two-way ANOVA
for repeated measures (group, time). In case of significant variations
in the time factor, with no group-time interaction, we subsequently
performed a t-test at each minute in
comparison with the baseline value in each group of patients. A two-way
ANOVA for repeated measures (group, test) was performed to analyze the
changes in parameters throughout the study. A group-test interaction
was the indicator of the difference in behavior between the two groups.
Finally, a three-way ANOVA (group, test, arterial site; data not shown)
was performed to compare behavior during CPT depending on the measured
artery (carotid or brachial). A P
value < 0.05 was considered significant.
| |
RESULTS |
Table 1 shows the clinical characteristics of both groups of patients.
Whereas body weight, height, and age did not differ, the blood pressure
measured with a mercury sphygmomanometer significantly differed,
although the mean value for DBP was only slightly increased in subjects
with borderline hypertension. Table 2 shows
the changes in mean values of blood pressure and heart rate
(automatically recorded with Dinamap) during the CPT. All the variables
of blood pressure (SBP, DBP, MBP, and PP) were significantly higher in patients with BHT (group factor: P < 0.001, P < 0.001, P < 0.001, and
P < 0.01, respectively). The basal
level of heart rate was higher in patients with BHT than in
normotensive subjects (P < 0.01).
The CPT increased all variables of blood pressure in both groups
(P < 0.001, P < 0.01, P < 0.001, and
P < 0.001, respectively), but heart
rate did not change during CPT. However, no group-time interaction was
observed. Figure 1 shows the SBP, DBP, PP,
and heart rate evolution during the CPT minute by minute. The group factor was significantly different for blood pressure but not for heart
rate. The latter remained unchanged throughout the test, whereas SBP
increased from the first minute until the end of the test. The same
finding was observed for PP, but only in normal subjects. DBP also
increased from the beginning of the stimulus but returned to baseline
after the 3rd minute. There was no group-time interaction, suggesting a
similar behavior between groups.
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Fig. 1.
Kinetics of systolic (SBP) and diastolic blood pressure (DBP), pulse
pressure (PP), and heart rate during cold pressor test (CPT) compared
with baseline in normal subjects ( ) and borderline hypertensive
(BHT) patients ( ). NS, not significant.
* P < 0.05;
** P < 0.01 vs.
baseline. For each variable, interaction is not significant.
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Table 3 shows the hemodynamic changes
observed for the carotid artery. Between-group differences
were observed for local SBP, DBP, and PP (higher in patients with BHT;
P < 0.001, P < 0.01, and
P < 0.01, respectively) as well as
CSC and DC (P < 0.05 and
P < 0.01, respectively). CPT
increased local SBP, DBP, PP, (Pk Pi), and
(Pk Pi)/PP and decreased the transit
time of the reflection wave
(Dtp), the relative stroke
change in diameter [(Ds Dd)/Dd],
CSC, and DC. Although CSC seemed to decrease less in patients with
BHT (due to differences in diameter behavior), a group-test interaction
was only observed for carotid artery Ds and
Dd, which
decreased in patients with BHT but increased in normal controls
(P < 0.05). The augmentation index
[(Pk Pi)/PP] increased more in
normal subjects (interaction: P < 0.05) from a negative value to a positive amplification, suggesting
a different hemodynamic behavior between groups at the central artery
level.
Table 4 shows the hemodynamic changes
observed for the brachial artery. Between-group differences were
observed for local SBP, DBP, and PP (higher in patients with BHT;
P < 0.001, P < 0.001, and
P < 0.05, respectively). CPT
increased local SBP, DBP, and PP and decreased
(Ds Dd),
(Ds Dd)/Dd,
CSC, and DC. For the two latter parameters, there was no group effect.
A group-test interaction was only observed for
(Ds Dd)/Dd
(P < 0.01) and for DC
(P < 0.01), which decreased less in
patients with BHT.
The three-way ANOVA (data not shown) showed a test-arterial site
interaction only for locally measured SBP
(P < 0.02) with a smaller increase
at the brachial artery site.
Figure 2 shows the relative change (%) in
DC, arterial distension
(Ds Dd), and local
PP during the CPT with respect to each group of patients and each
artery. The mechanism of the decrease in distensibility involves a
constant increase in PP, which is more pronounced in normal subjects
than in patients with BHT. A decrease in arterial distension is also
present but is more pronounced in normal subjects, particularly for the
brachial artery.
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Fig. 2.
Relative changes in distensibility coefficient, arterial distension
[systolic diameter
(Ds) minus
diastolic diameter
(Dd)],
and local PP in carotid (filled bars) and brachial arteries (open bars)
in normal subjects (A) and BHT
patients (B) during CPT.
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|
In summary, CPT increased all the local pressures and the timing of
reflection waves in both groups and decreased relative stroke change in
diameter and arterial distensibility at each arterial site. Intergroup
analysis showed that during the CPT, amplification of reflection waves
was higher in normal subjects than in patients with BHT, with an
increase in carotid diameters. Relative stroke change in brachial
diameter and brachial artery DC decreased more in normal subjects than
in patients with BHT. PP amplification, evaluated from the ratio of
brachial to carotid PP, decreased markedly during CPT in both groups
and reached similar values during CPT (Fig.
3).
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Fig. 3.
Ratio of brachial PP (PPb) to
carotid artery PP (PPc) in
baseline condition and during CPT in normal subjects () and BHT
patients (); au, arbitrary units. P < 0.01, baseline vs. CPT.
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| |
DISCUSSION |
CPT is a classic test of sympathetic activity causing arteriolar
vasoconstriction, resulting in an increase in blood pressure without a
change in heart rate. In the present study, we showed that CPT was
responsible for a disappearance of pulse pressure amplification as a
consequence of an earlier return of carotid wave reflections and an
increase in carotid pulse pressure. Arterial distensibility was reduced
at the site of the radial and carotid arteries, but a group effect was
observed only for the carotid artery. In addition, a lesser response
was noted in subjects with BHT than in controls.
CPT and pulse pressure amplification.
During the CPT, we have shown that blood pressure increased without a
significant difference between groups. Although larger increases were
found in several studies including borderline hypertensive subjects
(18, 24, 25), the present finding has already been shown by other
groups (26, 27, 30). Such discrepancies could be explained mainly by
methodological aspects, particularly differences in duration of
stimulus. However, even when blood pressure was measured minute by
minute, we did not observe any difference in responses between groups
(see Fig. 1, interaction NS). SBP increased in both
groups throughout the stimulus in comparison with baseline, except at
the 5th minute of recording in patients with BHT. With regard to DBP,
the increase was observed only until the 2nd minute in patients with
BHT and the 3rd minute in controls. However, this small difference may
be important to consider in terms of calculation of pulse pressure,
which increased in normal subjects but not in patients with BHT. In
previous studies, differences in intensity of stimulus and in the
timing of measurements have been responsible for discrepancies in
pulse-pressure calculations and, hence, in compliance determinations of
the radial artery (3, 12). In this study, according to average values
or minute-by-minute recordings, heart rate did not show any significant
variation, as already reported by others (1, 32, 37). Finally, one major limitation of this study is related to the intermediate duration
of hemodynamic changes observed during the 5-min CPT. However, even in
patients with BHT, the increase in SBP lasted until the beginning of
the 5th minute of the test, and our vascular examinations were always
finished during the first part of this 5th minute.
One of the major findings of this study is the behavior of the aortic
reflection waves during CPT. In normal subjects, as expected (7, 19,
28), the shape of the baseline carotid artery pressure curve was of
type C, whereas in patients with BHT, the baseline pressure curve was
of type A or B. Expressed in terms of the augmentation index
[(Pk Pi)/PP] and the delay to
Pi (absolute
Dtp, or relative to LVET), the
differences did not reach the statistically significant level. During
CPT, all the normal subjects presented a type B or A central pressure
curve, and the change in augmentation index was of higher amplitude
than in patients with BHT. It is well established that, for a given absorption coefficient of the arterial tree, reflection wave depends on
two principal factors: the length of the arterial tree, particularly until the reflection site(s), and the velocity of the wave travel (28,
29). With regard to the length of the arterial tree, the reflection
site(s) are considered as the embranchments (particularly at the level
of renal arteries) and bifurcation of the aorta (16) and, mostly, the
arteriolar network (20, 29), which directly depends on the status of
the arteriolar vasoconstriction. During CPT, as a
consequence of the increase in peripheral resistance, the arteriolar
site of reflection becomes closer to the heart and contributes to
enhance the impact of the backward wave on central pulse pressure. On
the other hand, it is well known that the pulse-wave velocity is
influenced not only by the arterial physical properties but also by the
level of blood pressure (29). Thus, due to the increase in blood
pressure observed during CPT, we can reasonably assume that the
pulse-wave velocity increased significantly and contributed to the
enhancement of reflection waves. Finally, the global effect of wave
reflections in both populations was a significant decrease in
Dtp and an increase in
(Pk Pi)/PP, indicating an earlier
return of the backward pressure wave and causing a higher carotid
systolic peak, which was even more pronounced in normal subjects than
in patients with BHT.
Subsequently, the major finding in both populations of subjects was the
disappearance of pulse-pressure amplification during CPT (Fig. 3). This
hemodynamic pattern is largely different from that observed during the
sympathetic activation produced by LBNP (31). During LBNP, an increase
in pulse-pressure amplification occurs because of a decrease in carotid
pulse pressure in relation to an acceleration of heart rate and a
shortening of LVET. During CPT, such a change was totally absent,
because there was no significant change in heart rate.
Changes in compliance and distensibility under CPT.
Until recent years, in most studies in the literature, compliance was
evaluated in vitro from arterial segments on which a steady pressure
was applied to determine the static pressure-diameter curve (29).
However, during such studies, when a sinusoidal transmural pressure
could be applied acutely, it was possible to determine dynamic
compliance at different arbitrary levels of steady transmural pressure
(2). In a given large artery, dynamic compliance is known to be
constantly lower than the corresponding static compliance because of
the frequency dependence of the viscosity of the arterial wall (2).
Subsequently, when two arteries were simultaneously studied and
compared in vitro, the same sinusoidal transmural pressure was applied
to determine the dynamic compliance of each artery. This methodology is
totally different from that of the dynamic compliance measurements in
clinical studies. In a given subject, when two different arteries are
compared, this comparison is obviously done for the same mean arterial
pressure (which is constant along the arterial tree) but at different
values of pulse pressure, because of the presence of pulse-pressure
amplification. Using this procedure, we showed that, both before and
during CPT, distensibility was reduced in subjects with BHT, but only
at the site of the carotid artery, not at the site of the brachial
artery. This finding clearly demonstrates that changes in
distensibility in vivo are influenced not only by the level of blood
pressure but also by the changes in the intrinsic properties of the
arterial wall. In a previous study, we compared in vitro the mechanical properties of the muscular radial artery and the musculoelastic internal mammary artery (6). We showed that under norepinephrine stimulation, the isobaric elastic modulus decreased in the former and
was unchanged in the latter, suggesting that the sympathetic response
is influenced by the baseline status of vascular structure and
function. Other hypotheses may arise taking into account the approach
of integrative physiology. It is possible that activation of
thermoreceptors in the skin during cold exposure sends afferent impulses to the central nervous system, which, in turn, may cause the
radial artery (close to the skin) and the carotid artery (away from the
skin) to respond in a significantly different manner, although this
suggestion results from study of the arteriolar splanchnic bed (33),
not large arteries.
In the case of large arteries studied under physiological conditions,
pulse pressure is known to be the mechanical signal producing an
increase in pulsatile diameter. Thus it is expected that the higher the
pulse pressure, the higher the pulsatile change of diameter. In
contrast with this simple logic, we observed that during CPT, the
increase in pulse pressure was associated with a significant decrease
(and not an increase) in pulsatile diameter. Thus, with the activation
of the autonomic nervous system produced by CPT, both a mechanical
(increase in pulse pressure) and a nonmechanical (decrease in pulsatile
diameter) alteration were obtained. In normal subjects, the two
mechanisms contributed to the decrease in distensibility during CPT,
particularly for the brachial artery (Fig. 2). In subjects with BHT,
only the increase in pulse pressure contributed to the decrease in
distensibility, resulting in a smaller change in arterial stiffness.
In conclusion, the present study has shown that the interpretation of
the distensibility changes of the large arteries is quite different in
situations of in vivo and in vitro experiments. In humans the exact
role of blood pressure should be evaluated by taking into account the
presence of pulse-pressure amplification. Pulse-pressure amplification
tends to disappear during CPT as a consequence of a higher increase in
carotid than in brachial pulse pressure. Such changes in normal
subjects are different from those in patients with BHT, possibly as a
consequence of a higher basal sympathetic tone in the latter.
| |
FOOTNOTES |
Address for reprint requests: M. Safar, Médecine 1, Hôpital Broussais, 96 rue Didot, 75014 Paris, France.
Received 14 November 1997; accepted in final form 10 April 1998.
| |
REFERENCES |
1.
Benetos, A.,
and
M. E. Safar.
Response to the cold pressor test in normotensive and hypertensive patients.
Am. J. Hypertens.
4:
627-629,
1991[Medline].
2.
Bergel, D. H.
The dynamic elastic properties of the arterial wall.
J. Physiol. (Lond.)
156:
458-469,
1961.
3.
Boutouyrie, P.,
P. Lacolley,
X. Girerd,
L. Beck,
M. Safar,
and
S. Laurent.
Sympathetic activation decreases medium-sized arterial compliance in humans.
Am. J. Physiol.
267 (Heart Circ. Physiol. 36):
H1368-H1376,
1994[Abstract/Free Full Text].
4.
Boutouyrie P., S. Laurent, A. Benetos, X. J. Girerd,
A. P. Hoeks, and M. E. Safar. Opposing effects
of ageing on distal and proximal large arteries in hypertensives.
J. Hypertens. 10, Suppl.: S87-S92, 1992.
5.
Calhoun, D. A.,
M. L. Mutinga,
A. S. Collins,
J. M. Wyss,
and
S. Oparil.
Normotensive blacks have heightened sympathetic response to cold pressor test.
Hypertension
22:
801-805,
1993[Abstract/Free Full Text].
6.
Chamiot-Clerc, P., X. Copie, J. F. Renaud, M. Safar,
and X. Girerd. Comparative reactivity and mechanic properties of
human isolated internal mammary and radial arteries.
Cardiovasc. Res. In press.
7.
Chen, C. H.,
C. T. Ting,
A. Nussbacher,
E. Nevo,
D. A. Kass,
P. Pak,
S. P. Wang,
M. S. Chang,
and
F. C. Yin.
Validation of carotid artery tonometry as a means of estimating augmentation index of ascending aortic pressure.
Hypertension
27:
168-175,
1996[Abstract/Free Full Text].
8.
Cuddy, R. P.,
H. Smulyan,
and
J. F. Keighley.
Hemodynamic and catecholamine changes during a standard cold pressor test.
Am. Heart J.
71:
446-454,
1966[Medline].
9.
Dobrin, P. B.,
and
A. A. Rovick.
Influence of vascular smooth muscle on contractile mechanics and elasticity of arteries.
Am. J. Physiol.
217:
1644-1651,
1969.
10.
Girerd, X., X. Chanudet, P. Larroque, R. Clement, B. Laloux, and
M. Safar. Early arterial modifications in young patients with
borderline hypertension. J. Hypertens.
7, Suppl.: S45-S47, 1989.
11.
Hoeks, A. P.,
P. J. Brands,
F. A. Smeets,
and
R. S. Reneman.
Assessment of the distensibility of superficial arteries.
Ultrasound Med. Biol.
16:
121-128,
1990[Medline].
12.
Joannides, R.,
V. Richard,
N. Moore,
M. Godin,
and
C. Thuillez.
Influence of sympathetic tone on mechanical properties of muscular arteries in humans.
Am. J. Physiol.
268 (Heart Circ. Physiol. 37):
H794-H801,
1995[Abstract/Free Full Text].
13.
Kelly, R.,
C. Hayward,
J. Ganis,
J. Daley,
A. Avolio,
and
M. F. O'Rourke.
Non-invasive registration of the arterial pressure pulse waveform using high-fidelity aplanation tonometry.
J. Vasc. Med. Biol.
1:
142-149,
1989.
14.
Kool, M. J.,
A. P. Hoeks,
H. A. Struijker-Boudier,
R. S. Reneman,
and
L. M. Van Bortel.
Short and long-term effects of smoking on arterial properties in habitual smokers.
J. Am. Coll. Cardiol.
22:
1881-1886,
1993[Abstract].
15.
Krooker, E. J.,
and
E. H. Wood.
Comparison of simultaneously recorded central and peripheral arterial pressure pulses during rest, exercise, and tilted position in man.
Circ. Res.
3:
623-632,
1995.
16.
Latham, R. D.,
M. Westerhof,
P. Skipema,
B. J. Rubal,
P. Reuderink,
and
J. P. Murgo.
Regional wave travel and reflections along human aorta: a study with 6 simultaneous micromanometric pressures.
Circulation
72:
1257-1269,
1985[Abstract/Free Full Text].
17.
Laurent, S.,
B. Caviezel,
L. Beck,
X. Girerd,
E. Billaud,
P. Boutouyrie,
A. Hoeks,
and
M. Safar.
Carotid artery distensibility and distending pressure in hypertensive humans.
Hypertension
23:
878-883,
1994[Abstract/Free Full Text].
18.
Letizia, C.,
S. Cerci,
A. De Ciocchis,
C. D'Ambrosio,
L. Scuro,
and
D. Scavo.
Plasma endothelin-1 levels in normotensive and borderline hypertensive subjects during a standard cold pressor test.
J. Hum. Hypertens.
9:
903-907,
1995[Medline].
19.
London, G.,
A. Guerin,
B. Pannier,
S. Marchais,
A. Benetos,
and
M. Safar.
Increased systolic pressure in chronic uremia. Role of arterial wave reflections.
Hypertension
20:
10-19,
1992[Abstract/Free Full Text].
20.
London, G.,
A. P. Guerin,
B. Pannier,
S. J. Marchais,
and
M. Stimpel.
Influence of sex on arterial hemodynamics and blood pressure. Role of body height.
Hypertension
26:
514-519,
1995[Abstract/Free Full Text].
21.
London, G.,
B. Pannier,
E. Vicaut,
A. P. Guerin,
S. J. Marchais,
M. E. Safar,
and
J. L. Cuche.
Antihypertensive effects and arterial haemodynamic alterations during angiotensin converting enzyme inhibition.
J. Hypertens.
14:
1139-1146,
1996[Medline].
22.
Marchais, S. J.,
A. P. Guerin,
B. M. Pannier,
B. I. Levy,
M. E. Safar,
and
G. M. London.
Wave reflections and cardiac hypertrophy in chronic uremia. Influence of body size.
Hypertension
22:
876-883,
1993[Abstract/Free Full Text].
23.
Mark, A. L.,
and
G. Mancia.
Cardiopulmonary baroreflexes in humans.
In: Handbook of Physiology. The Cardiovascular System. Peripheral Circulation and Organ Blood Flow. Bethesda, MD: Am. Physiol. Soc., 1983, sect. 2, vol. III, pt. 2, chapt. 21, p. 795-813.
24.
Matsukawa, T.,
E. Gotoh,
S. Uneda,
E. Miyajima,
H. Shionoiri,
O. Tochikubo,
and
M. Ishii.
Augmented sympathetic nerve activity in response to stress in young borderline hypertensive men.
Acta Physiol. Scand.
141:
157-165,
1991[Medline].
25.
Miyajima, E., Y. Yamada, T. Matsukawa, O. Tochikubo, M. Ishii,
and Y. Kaneko. Neurogenic abnormalities in young borderline
hypertensives. Clin. Exp. Hypertens.
10, Suppl. 1:
209-223, 1988.
26.
Murakami, E.,
K. Hiwada,
and
T. Kokubu.
Pathophysiological characteristics of labile hypertensive patients determined by the cold pressor test.
Jpn. Circ. J.
44:
438-442,
1980[Medline].
27.
Murakami, M.,
H. Suzuki,
M. Naitoh,
H. Nakamoto,
A. Ichihara,
A. Matsumoto,
E. Takeshita,
Y. Kanno,
and
T. Saruta.
Evidence for abnormalities in the parasympathetic nerve-mediated reflexes in borderline hypertension.
Hypertens. Res. Clin. Exp.
16:
185-190,
1993.
28.
Murgo, J. P.,
N. Westerhof,
and
S. A. Giolma.
Aortic input impedance in normal man: relationship to pressure wave forms.
Circulation
62:
105-116,
1980[Free Full Text].
29.
Nichols, W. V.,
and
M. F. O'Rourke.
McDonald's Blood Flow in Arteries: Theoretic, Experimental, and Clinical Principles (3rd ed.), edited by E. Arnold. London, UK: Melbourne, 1990, p. 77-142, 216-269, 398-411.
30.
Ostergren, J.,
T. Kahan,
P. Hjemdahl,
B. Fagrell,
U. de Faire,
and
K. Lindvall.
Effects of sympatho-adrenal activation on the finger microcirculation in mild hypertension.
J. Hum. Hypertens.
6:
169-173,
1992[Medline].
31.
Pannier, B.,
M. A. Slama,
G. M. London,
M. E. Safar,
and
J. L. Cuche.
Carotid arterial hemodynamics in response to LBNP in normal subjects: methodological aspects.
J. Appl. Physiol.
79:
1546-1555,
1995[Abstract/Free Full Text].
32.
Puybasset, L.,
P. Lacolley,
S. T. Laurent,
F. Mignon,
E. Billaud,
J. L. Cuche,
E. Comoy,
and
M. Safar.
Effects of clonidine on plasma catecholamine and neuropeptide Y in hypertensive patients at rest and during stress.
J. Cardiovasc. Pharmacol.
21:
912-919,
1993[Medline].
33.
Riedel, W.,
M. Iriki,
and
E. Simon.
Regional differentiation of sympathetic activity during peripheral heating and cooling in anesthetized rabbits.
Pflügers Arch.
332:
239-247,
1972[Medline].
34.
Safar, M. E.,
Y. A. Weiss,
J. A. Levenson,
G. M. London,
and
P. L. Milliez.
Hemodynamic study of 85 patients with borderline hypertension.
Am. J. Cardiol.
31:
315-319,
1973[Medline].
35.
Van Merode, T.,
P. J. Brands,
A. P. Hoeks,
and
R. S. Reneman.
Faster ageing of the carotid artery bifurcation in borderline hypertensive subjects.
J. Hypertens.
11:
171-176,
1993[Medline].
36.
Victor, R. G.,
W. N. Leimbach, Jr.,
D. R. Seals,
B. G. Wallin,
and
A. L. Mark.
Effects of the cold pressor test on muscle sympathetic nerve activity in humans.
Hypertension
9:
429-436,
1987[Abstract/Free Full Text].
37.
Weise, F.,
D. Laude,
A. Girard,
P. Zitoun,
J. P. Siche,
and
J. L. Elghozi.
Effects of the cold pressor test on short-term fluctuations of finger arterial blood pressure and heart rate in normal subjects.
Clin. Auton. Res.
3:
303-310,
1993[Medline].
Am J Physiol Heart Circ Physiol 275(2):H409-H415
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Abstract
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