(Hypertension. 1999;33:1195-1200.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Effects of Age and Gender on Autonomic Control of Blood Pressure Dynamics
From the Hebrew Rehabilitation Center for Aged Research and Training Institute (S.R.B., L.A.L., R.J.M., D.K.K., M.G.), Beth Israel/Deaconess Medical Center, Departments of Medicine (L.A.L., G.A., E.L.K.) and Anesthesia (S.R.B.), Harvard Medical School, Boston, Mass; and Quest Diagnostics Nichols Institute (J.C.N.), San Juan Capistrano, Calif.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract—Both age and gender influence cardiovascular autonomic control, which in turn may influence the ability to withstand adverse cardiac events and respond to orthostatic stress. The purpose of this study was (1) to quantify age- and gender- related alterations in autonomic control of blood pressure (BP) and (2) to examine the impact of these autonomic alterations on BP response to orthostatic stress. We measured continuous BP and R-R intervals and vasoactive peptide levels in the supine and 60° head-up tilt positions during paced respiration (0.25 Hz) in 89 carefully screened healthy subjects (41 men, 48 women, aged 20 to 83 years). Data were analyzed by gender (age adjusted) and by age group (gender adjusted). During tilt, women had greater decreases in systolic BP than men (-10.2±2 versus -1.2±3 mm Hg; P=0.02) and smaller increases in low-frequency (sympathetically mediated) BP power (P=0.02). Upright plasma norepinephrine was lower in women (P=0.02). Women had greater supine high-frequency R-R interval power than men (P=0.0001). In elderly subjects, the tilt-induced increase in low-frequency BP power was also diminished (P=0.01), despite higher supine (P=0.02) and similar upright norepinephrine levels compared with younger subjects. Thus, healthy women have less sympathetic influence on BP and greater parasympathetic influence on R-R interval than men. Elderly subjects also have reduced sympathetic influence on BP, but this appears to be more consistent with a reduction in vasomotor sympathetic responsiveness.
Key Words: sympathetic nervous system • norepinephrine • spectral analysis • hypotension
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Analyses of the beat-to-beat variability of cardiac R-R intervals have been used to quantify alterations in autonomic function and predict adverse clinical events.1 2 Since both age and gender have a profound influence on the risk of cardiovascular disease and death, it is important to understand the effects of healthy aging and gender on autonomic control of cardiovascular function. Previous studies have shown reductions in heart rate (HR) variability with aging3 4 and increases in high-frequency HR variability in women compared with men.5 6 7 Since many studies did not rigorously screen subjects to exclude occult cardiovascular disease, it is not known whether abnormalities in short-term autonomic control of HR reflect subclinical cardiovascular disease or whether they represent "normal" age- or gender-related alterations in autonomic function.
The effects of age and gender on beat-to-beat blood pressure (BP) dynamics have been less well studied, and it is not known whether changes in the autonomic regulation of beat-to-beat BP are associated with hemodynamic impairment. Therefore, we asked the following questions: (1) Are there specific age- and gender-related alterations in the autonomic control of beat-to-beat BP dynamics in healthy individuals free of cardiovascular disease? (2) If so, what are the hemodynamic consequences of these changes during orthostatic stress?
We used spectral analysis of continuous BP and R-R interval time series obtained in the supine and head-up tilt positions to assess alterations in the short-term autonomic regulation of BP and R-R. Spectral analysis decomposes cardiovascular signals into their frequency components and quantifies the power of each component.8 During paced breathing at 0.25 Hz in the supine position, high-frequency R-R interval power (0.15 to 0.50 Hz) quantifies the amplitude of the vagally mediated respiratory sinus arrhythmia. During upright tilt, increases in low-frequency BP power ("Mayer waves," 0.04 to 0.15 Hz) represent baroreflex-mediated increases in sympathetic vasomotor activity. The degree to which low-frequency BP oscillations are associated with oscillations in R-R interval at the same frequency (transfer magnitude) was used as a measure of cardiovagal baroreflex gain.9 Finally, we examined plasma norepinephrine level and levels of other circulating vasoactive peptides to determine their potential relationship to hemodynamic changes during orthostatic stress.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Subjects
One hundred forty-four potential subjects were recruited from the local community through newspaper advertisements and the Harvard Cooperative Program on Aging subject registry. After an initial telephone screen, subjects underwent a history and physical examination, complete blood count, chemistry and lipid profile, and ECG. Subjects aged >40 years also performed a graded exercise stress test. Exclusion criteria included evidence of cardiovascular or other diseases, tobacco or alcohol use, obesity (body mass index >30 kg/m2), hypertension (systolic BP >140 mm Hg), and use of medication other than oral contraceptives (n=8). A total of 34 subjects were ineligible after screening, and 15 decided to withdraw, leaving 95 subjects who completed the study. Six of these subjects were excluded during data analysis because of frequent ectopy during prolonged cardiac monitoring. Therefore, the final sample included 89 healthy subjects. The study was approved by the Institutional Review Board of the Hebrew Rehabilitation Center for Aged, and all subjects provided informed consent.
Instrumentation
Subjects reported to the Cardiovascular
Research Laboratory at 7:30 AM on the morning of the study
in the fasting state. Premenopausal women were studied between days 7
and 14 of their menstrual cycle. While the patient was supine on a tilt
table, an intravenous catheter was placed in the right
antecubital vein for blood sampling. Electrodes were attached to the
chest for continuous recording of the ECG. The right arm was
kept level with the right atrium, and a noninvasive tonometric BP
transducer, connected to a Colin Electronics BP monitor, was
strapped over the right radial artery. The sphygmomanometric cuff of an
oscillometric BP recording device for calibration of the
tonometric transducer was attached to the upper right arm. Forearm
blood flow was determined on the other arm by venous occlusion
plethysmography with the use of a Hokanson plethysmograph and the
procedure of Whitney.10 Vascular resistance was calculated
from the mean arterial pressure divided by forearm
blood flow.
A continuous respiration signal was recorded by an inductive plethysmograph (Respitrace, Ambulatory Monitoring) from 2 elastic respiratory transducer bands placed around the chest and abdomen. The Respitrace output was calibrated by having subjects exhale and inhale to fill and empty an 800-mL spirometer bag.11 Baseline minute ventilation was calculated during 3 minutes of spontaneous breathing. During paced breathing, subjects followed a tape-recorded auditory signal and line on an oscilloscope screen to control respiratory frequency at 15 breaths per minute (0.25 Hz) and hold minute ventilation constant.
Experimental Protocol
Subjects rested supine for 30 minutes to reach equilibrium.
Continuous ECG, BP, and respiratory data and 2 baseline blood samples
were then collected during 8 minutes of supine rest, while subjects
performed paced breathing. The bed was then tilted to the 60° head-up
position over 30 seconds. Between 5 and 15 minutes in the upright
position, subjects again performed paced breathing while continuous
ECG, BP, and respiratory data were collected. Blood samples were
obtained at 15 minutes of upright tilt.
Vasoactive Hormone and Peptide Assays
Plasma was collected in tubes containing glutathione for
the norepinephrine assay and in tubes containing EDTA and
aprotinin for measurements of endothelin, renin (renin peptide and
plasma renin activity), and aldosterone. Plasma was stored
at -70°C until assayed. All assays were performed by the Corning
Nichols Laboratory.
Norepinephrine was measured in a plasma extract by high-performance liquid chromatography with the use of a cation exchange column, an acetonitrile/phosphate buffer mobile phase, and electrochemical detection, with an interassay coefficient of variation (CV) of 3.9%. Endothelin was measured in an extract of plasma by a double-antibody radioimmunoassay method with endothelin-1 standards and an interassay CV of 9.1%. Renin peptide (immunoreactive renin) was measured in plasma by a direct 2-site immunoradiometric assay with an interassay CV of 7.1%. Renin activity (enzymatic) was measured by the rate of angiotensin-1 formation from angiotensinogen by renin in the presence of angiotensin-converting enzyme and angiotensinase inhibitors. The interassay CV was 15.7%. Aldosterone was measured by radioimmunoassay after solvent extraction and celite column chromatography for purification of aldosterone, with an interassay CV of 14.5%.
Data Processing
ECG, BP, and respiratory data were digitized at 250 Hz and
displayed in real time on a personal computer (Windaq, Dataq
Instruments). Continuous ECG and BP data before and during tilt were
edited offline for artifact and ectopy with the use of an automated
arrhythmia detection program for the ECG and manual editing for
BP. Eight-minute data segments during paced breathing, with the subject
supine and in the tilt position, were used for the
analysis.
Beat-to-beat R-R intervals were determined from the R wave of the ECG, and beat-to-beat systolic and diastolic BPs were derived from the maximum and minimum of the arterial pressure waveform. Each R-R systolic and diastolic BP time series was interpolated by cubic spline function and resampled at 2 Hz to obtain equidistant time intervals. The resampled series were analyzed with a fast Fourier transform algorithm.12 The areas under the power spectra in the Mayer wave and respiratory frequencies (defined as 0.04 to 0.15 and 0.15 to 0.50 Hz, respectively) were integrated and used for statistical comparisons. HR was calculated as the reciprocal of the R-R interval (in seconds), multiplied by 60. Mean HRs and BPs were determined from the 8-minute data segments during supine and upright time periods.
Statistical Analysis
Two separate analyses were performed, 1 by age group (20
to 39, 40 to 59, and 
60 years) and 1 by gender. We compared baseline
characteristics of groups of subjects with ANCOVA, controlling for
either age or gender.13 Supine and tilt
cardiovascular variables and spectral powers were
compared between the groups with 2-way (group and time)
repeated-measures ANCOVA. Multiple linear regression was also used to
determine factors independently associated with changes in BP power
during upright tilt. All spectral data were natural log transformed to
normalize their distributions. Data are expressed as untransformed
mean±SE values. An 
level 
0.05 was used to determine statistical
significance.
To characterize the cardiovagal baroreflex, we examined the linear relation (coherence) and strength of that relation (transfer magnitude) between systolic BP (input signal) and R-R interval (output signal) fluctuations in the low-frequency range (0.04 to 0.15 Hz) during supine and upright tilt conditions. We calculated the coherence and transfer magnitudes between the signals using the technique of Saul et al,9 with paced rather than random breathing. All analyses were performed with DaDisp software on a personal computer. Coherence was calculated from the cross-spectra and autospectra of the time series according to the following formula: ||Cross-Spectra||2/||Input Signal Autospectrum||x||Output Signal Autospectrum||. The signals were considered coherent over the frequencies at which coherence values were >0.5.9 The complex transfer function was calculated by dividing the cross-spectrum by the input autospectrum. The transfer magnitude was then derived for each subject over the low-frequency range meeting the coherence criterion.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Effects of Age
Baseline Characteristics
As shown in Table 1, forearm vascular resistance (FVR) was greater in the old, and plasma norepinephrine levels were greater with increasing age. However, low-frequency diastolic BP power was lower in the older group than in the middle-aged and young. High-frequency R-R interval power and transfer magnitude were also lower in the oldest age group.
|
Response to Tilt
The responses to head-up tilt
were similar whether absolute or relative changes were
analyzed; therefore, only absolute changes are reported as
shown in Table 2. HR and FVR increased during tilt (P=0.001
and P0.0003, respectively), and HR increased to a greater
extent in the young than in middle-aged and old groups.
|
In response to upright tilt, low-frequency systolic and diastolic BP power increased in all groups (P<0.0003). The increase in diastolic power was greater in the young than in middle-aged and old groups (Table 2). While subjects were in the upright position, both low-frequency systolic (P=0.01) and diastolic (P=0.0001) BP power were lower in the old group than in the middle-aged and young (Figure 1). Plasma norepinephrine levels increased to the same extent in all groups (Table 2 and Figure 1).
|
High-frequency R-R interval power fell during tilt in all ages (P<0.02) but to a significantly smaller extent in the middle-aged and old subjects than in the young group (P=0.001). There was a similar decline in transfer magnitude with posture change at all ages (P<0.04).
Direct renin increased with posture change in the young and middle-aged groups (P<0.006) but not to a significant extent in the old (P<0.03 for old compared with middle-aged and young groups). Plasma renin activity increased with posture change in all groups (P<0.006). Aldosterone increased in the middle-aged and old groups (P<0.0001) but not in the young. However, changes in aldosterone levels were not significantly different between groups.
Effects of Gender
Baseline Characteristics
As shown in Table 3, women had
smaller body mass index, higher basal HR, and greater high-frequency
R-R interval power than men. There were no differences in other
baseline hemodynamics, spectral powers, or circulating
vasoactive peptide levels.
|
Response to Tilt
As shown in Table 4, women had
a significant decline in systolic BP during tilt
(P=0.0001), while men did not. However, HR and FVR increased
by the same extent in women and men (P<0.0001 for each
variable). In the upright position, low-frequency systolic
and diastolic BP powers and plasma
norepinephrine levels increased less and achieved lower
values in women than in men (Table 4 and Figure 2). There was a trend toward greater
reduction in high-frequency R-R power in women than in men
(P=0.10). Transfer magnitudes decreased
(P=0.0002), and aldosterone, direct renin, and
plasma renin activity increased to a similar extent in both genders
during head-up tilt.
|
|
Multivariate Analysis
Multiple linear regression analyses examining the
effects of age, genders, body mass index, and baseline BPs and R-Rs on
changes in BP power during upright tilt revealed that gender alone was
related to the change in systolic BP power (P=0.02),
and both age (P=0.0068) and gender (P=0.02) were
related to the change in diastolic BP power during tilt.
There was no age and gender interaction, indicating that gender-related
differences in BP dynamics were similar across all age groups.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Principal Findings
The results of this study indicate that both healthy aging and female gender are associated with reduced low-frequency beat-to-beat BP oscillations during orthostatic stress. These vasomotor oscillations, also called Mayer waves, are thought to represent the effects of baroreflex-mediated sympathetic outflow on the vasculature.14 Their attenuation with age and female gender appears to be due to different mechanisms. In elderly subjects, supine resting plasma norepinephrine levels were elevated, and the norepinephrine response to tilt was the same as that in the young. In contrast, women had lower plasma norepinephrine responses to tilt than men and a corresponding reduction in sympathetically mediated low-frequency vasomotor oscillations.
Second, the results show a striking dissociation between changes in beat-to-beat BP dynamics and changes in mean levels of forearm vascular tone. Despite a blunted increase in the amplitude of low-frequency beat-to-beat BP oscillations during head-up tilt, both elderly and female subjects were able to increase mean levels of FVR to the same extent as their younger or male counterparts.
Third, we found that women had greater declines in systolic BP during tilt than men. This was not explained by differences in HR, cardiovagal baroreflex gain, or various neurohumoral modulators of vascular tone and volume status, including plasma renin, aldosterone, and endothelin. Given their blunted plasma norepinephrine response, orthostatic hypotension in women may result from reduced cardiac inotropy or reduced systemic rather than regional (forearm) vasoreactivity.
Finally, this study confirmed our previous findings that high-frequency R-R variability in the supine position, a marker of the vagally mediated respiratory sinus arrhythmia, is reduced as a function of age15 but elevated in women across all ages.5 Thus, women appear to have a more favorable autonomic profile of reduced sympathetic and enhanced parasympathetic activity than men, but possibly at the expense of mild orthostatic hypotension.
Effects of Healthy Aging on BP Variability
Although Taylor et al16 reported supine,
resting low-frequency diastolic BP variability to be lower
in healthy older versus younger males, only 1 study to our knowledge
examined the effect of aging on beat-to-beat BP variability during
orthostatic stress.17 This study compared
preadolescents (aged 10 to 15 years) to young adults (aged 20 to 40
years) and elderly subjects (aged 70 to 90 years); however, the elderly
were not screened with exercise tests to exclude the possibility of
occult cardiovascular disease. Consistent with
our results, there was an increase in low-frequency (referred to as
"mid-frequency" in their study) systolic and
diastolic BP power during upright posture in all age
groups, but a smaller increase in the elderly subjects.
Effects of Gender on BP Variability
Little is known about the effects of gender on BP dynamics.
We previously found that healthy postmenopausal women taking estrogen
replacement therapy had reduced low-frequency BP variability after
head-up tilt or a meal, compared with untreated age-matched female
controls.18 It is possible that estrogen reduces
beat-to-beat BP variability by increasing baroreflex
sensitivity.19 If estrogen was solely responsible for
reduced BP variability, however, one would expect to see less of a
gender-related effect on BP dynamics after menopause or differences in
baroreflex sensitivity between premenopausal women and men. This
was not found in the present study. There may be an intrinsic
difference in BP regulation in women compared with men.
Differing Effects of Age and Gender
In contrast to the parallel age-related decline in both
low-frequency BP power in the tilted position (a measure of sympathetic
activity) and high-frequency R-R interval power in the supine position
(a measure of parasympathetic activity), gender affects these measures
in opposite directions, independent of age. The effect of aging might
be explained by the known age-related reduction in sympathetic
vasomotor responsiveness20 and reduced respiratory sinus
arrhythmia,15 which would reduce both
low-frequency BP oscillations and high-frequency R-R
interval oscillations in a parallel fashion. In contrast,
female gender is associated with reduced muscle sympathetic nerve
activity and plasma norepinephrine concentrations at
rest21 and, as we have shown, reduced plasma
norepinephrine levels during orthostatic
stress. Reductions in sympathetic activity produced by ß-blockade are
well known to enhance the respiratory sinus arrhythmia,
possibly because sympathetic activity has a restraining influence on
vagal modulation of HR.22 In women, this could explain why
reduced low-frequency BP variability (a measure of sympathetic
activity) is associated with enhanced high-frequency R-R interval
variability (the respiratory sinus arrhythmia).
Strengths and Weaknesses
The present study is limited by the absence of direct
measures of cardiac output, systemic vascular resistance, and blood
volume and by its reliance on circulating plasma
norepinephrine concentration, which is an indirect measure
of sympathetic nervous system activity. Nevertheless, this study
provides novel data showing that healthy women have less sympathetic
influence on BP and greater parasympathetic influence on R-R interval
than men, despite similar spontaneous baroreflex gain. Since high
sympathetic activity23 and low parasympathetic
activity1 2 are associated with
cardiovascular disease morbidity and mortality, the
favorable autonomic profile seen in women may be related to their
delayed onset of cardiovascular disease and increased
longevity compared with men.
|
Acknowledgments |
|---|
This study was supported by the Hebrew Rehabilitation Center for Aged, Quest Diagnostics Nichols Institute, a Brookdale Foundation grant, and Public Health Service grants AGO4390, AG14420, and AGO8812 from the National Institute on Aging, Bethesda, Md. Dr Lipsitz holds the Irving and Edyth S. Usen and Family Chair in Geriatric Medicine at the Hebrew Rehabilitation Center for Aged.
|
Footnotes |
|---|
Reprint requests to Lewis A. Lipsitz, MD, Hebrew Rehabilitation Center for Aged, 1200 Centre St, Boston, MA 02131.
Received October 13, 1998; first decision December 7, 1998; accepted January 12, 1999.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Bigger JT, Fleiss JL, Steinman RC, Rolnitzky LM, Schneider WJ, Stein PK. RR variability in healthy, middle-aged persons compared with patients with chronic coronary heart disease or recent acute myocardial infarction. Circulation. 1995;91:1939–1943.
2.
Tsuji H, Larson MG, Venditti FJ, Manders ES, Evans JC,
Feldman CL, Levy D. Impact of reduced heart rate variability on risk
for cardiac events: the Framingham Heart Study. Circulation. 1996;94:2850–2855.
3.
Hellman JB, Stacy RW. Variation of respiratory sinus
arrhythmia with age. J Appl Physiol. 1976;41:734–738.
4. Schwartz JB, Gibb WJ, Tran T. Aging effects on heart rate variation. J Gerontol. 1991;46:M99–M106.[Abstract]
5. Ryan SM, Goldberger AL, Pincus SM, Mietus J, Lipsitz LA. Gender and age-related differences in heart rate dynamics: are women more complex than men? J Am Coll Cardiol.. 1994;24:1700–1707.[Abstract]
6. Liao D, Barnes RW, Chambless LE, Simpson RJ Jr, Sorlie P, Heiss G. Age, race, and sex differences in autonomic cardiac function measured by spectral analysis of heart rate variability: the ARIC Study. Am J Cardiol. 1995;76:906–912.[Medline] [Order article via Infotrieve]
7.
Huikuri HV, Pikkujamsa SM, Airaksinen J, Ikaheimo MJ,
Rantala AO, Kauma H, Lilja M, Kesaniemi A. Sex-related differences in
autonomic modulation of heart rate in middle-aged subjects.
Circulation. 1996;94:122–125.
8.
Malliani A, Pagani M, Lombardi F, Cerutti S.
Cardiovascular neural regulation explored in the
frequency domain. Circulation. 1991;84:482–492.
9.
Saul JP, Berger RD, Albrecht P, Stein SP, Chen MH,
Cohen, RJ. Transfer function analysis of the circulation:
unique insights into cardiovascular regulation.
Am J Physiol. 1991;261:H1231–H1245.
10. Whitney RJ. The measurement of volume changes in human limbs. J Physiol (Lond). 1953;121:1–27.
11. Sackner JD, Nixon AJ, Davis B, Atkins N, Sackner MA. Non-invasive measurement of ventilation during exercise using a respiratory inductive plethysmograph, I. Am Rev Respir Dis.. 1980;122:867–871.[Medline] [Order article via Infotrieve]
12. Moody GB, Mark RG. The MIT-BIH Arrhythmia Database on CD-ROM, and software for use with it. In: Ripley KL, ed. Computers in Cardiology. Los Alamos, NM: IEEE Computer Society Press; 1990:185–188.
13. SAS II. SAS Technical Report P-229 SAS/STAT Software: Changes and Enhancement, Release 6.07. Cary, NC: SAS Institute, Inc; 1992:287–3681.
14.
Pagani M, Montano N, Porta A, Malliani A, Abboud FM,
Birkett C, Somers VK. Relationship between spectral components of
cardiovascular variabilities and direct measures of
muscle sympathetic nerve activity in humans. Circulation. 1997;95:1441–1448.
15.
Lipsitz LA, Mietus J, Moody GB, Goldberger AL. Spectral
characteristics of heart rate variability before and during postural
tilt: relations to aging and risk of syncope. Circulation. 1990;81:1803–1810.
16. Taylor JA, Williams TD, Seals DR, Davy KP. Low-frequency arterial pressure fluctuations do not reflect sympathetic outflow: gender and age differences. Am J Physiol. 1998;274:H1194–H1201.
17.
Veerman DP, Imholz BPM, Wieling W, Karemaker JM, van
Montfrans GA. Effects of aging on blood pressure variability in resting
conditions. Hypertension. 1994;24:120–130.
18.
Lipsitz LA, Connelly CM, Kelley-Gagnon MM, Kiely DK,
Morin RJ. Effects of chronic estrogen replacement therapy on
beat-to-beat blood pressure dynamics in healthy postmenopausal women.
Hypertension. 1995;26:711–715.
19. De Meersman RE, Zion AS, Giardina EGV, Weir JP, Lieberman JS, Downey JA. Estrogen replacement, vascular distensibility, and blood pressures in postmenopausal women. Am J Physiol. 1998;274:H1539–H1544.
20.
Hogikyan RV, Supiano MA. Arterial
alpha-adrenergic responsiveness is decreased and SNS activity is
increased in older humans. Am J Physiol. 1994;266:E717–E724.
21.
Ng AV, Callister R, Johnson DG, Seals DR. Age and
gender influence muscle sympathetic nerve activity at rest in healthy
humans. Hypertension. 1993;21:498–503.
22.
Coker R, Koziell A, Oliver C, Smith SE. Does the
sympathetic nervous system influence sinus arrhythmia in man?
Evidence from combined autonomic blockade. J Physiol. 1984;356:459–464.
23. Julius S, Nesbitt, S. Clinical consequences of the autonomic imbalance in hypertension and congestive heart failure. Scand Cardiovasc J Suppl. 1998;47:23–30.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  M. E. J. Lott, C. Hogeman, M. Herr, M. Bhagat, and L. I. Sinoway Sex differences in limb vasoconstriction responses to increases in transmural pressures Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H186 - H194. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. H. Huxley Sex and the cardiovascular system: the intriguing tale of how women and men regulate cardiovascular function differently Advan Physiol Educ, March 1, 2007; 31(1): 17 - 22. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Jones, A. Beda, A. M.V. Ward, C. Osmond, D. I.W. Phillips, V. M. Moore, and D. M. Simpson Size at Birth and Autonomic Function During Psychological Stress Hypertension, March 1, 2007; 49(3): 548 - 555. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Lavi, O. Nevo, I. Thaler, R. Rosenfeld, L. Dayan, N. Hirshoren, L. Gepstein, and G. Jacob Effect of aging on the cardiovascular regulatory systems in healthy women Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2007; 292(2): R788 - R793. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. A. Lipsitz, I. Iloputaife, M. Gagnon, D. K. Kiely, and J. M. Serrador Enhanced Vasoreactivity and Its Response to Antihypertensive Therapy in Hypertensive Elderly Women Hypertension, March 1, 2006; 47(3): 377 - 383. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
Q. Fu, S. Witkowski, K. Okazaki, and B. D. Levine Effects of gender and hypovolemia on sympathetic neural responses to orthostatic stress Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2005; 289(1): R109 - R116. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Tank, A. Diedrich, E. Szczech, F. C. Luft, and J. Jordan Baroreflex Regulation of Heart Rate and Sympathetic Vasomotor Tone in Women and Men Hypertension, June 1, 2005; 45(6): 1159 - 1164. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Tank Does Aging Cause Women to be More Sympathetic Than Men? Hypertension, April 1, 2005; 45(4): 489 - 490. [Full Text] [PDF]
|
|
|
|
 |
|
 D. D. Christou, P. P. Jones, J. Jordan, A. Diedrich, D. Robertson, and D. R. Seals Women Have Lower Tonic Autonomic Support of Arterial Blood Pressure and Less Effective Baroreflex Buffering Than Men Circulation, February 1, 2005; 111(4): 494 - 498. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Laitinen, L. Niskanen, G. Geelen, E. Lansimies, and J. Hartikainen Age dependency of cardiovascular autonomic responses to head-up tilt in healthy subjects J Appl Physiol, June 1, 2004; 96(6): 2333 - 2340. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Schroeder, F. Adams, M. Boschmann, J. Tank, S. Haertter, A. Diedrich, I. Biaggioni, F. C. Luft, and J. Jordan Phenotypical evidence for a gender difference in cardiac norepinephrine transporter function Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2004; 286(5): R851 - R856. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. A. Lipsitz Physiological Complexity, Aging, and the Path to Frailty Sci. Aging Knowl. Environ., April 21, 2004; 2004(16): pe16 - pe16. [Abstract] [Full Text]
|
|
|
|
 |
|
 S. Mukai, M. Gagnon, I. Iloputaife, J. W. Hamner, and L. A. Lipsitz Effect of Systolic Blood Pressure and Carotid Stiffness on Baroreflex Gain in Elderly Subjects J. Gerontol. A Biol. Sci. Med. Sci., July 1, 2003; 58(7): M626 - 630. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Lucini, G. S. Mela, A. Malliani, and M. Pagani Impairment in Cardiac Autonomic Regulation Preceding Arterial Hypertension in Humans: Insights From Spectral Analysis of Beat-by-Beat Cardiovascular Variability Circulation, November 19, 2002; 106(21): 2673 - 2679. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A Cohen and J A. Taylor Short-term cardiovascular oscillations in man: measuring and modelling the physiologies J. Physiol., August 1, 2002; 542(3): 669 - 683. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Geelen, T. Laitinen, J. Hartikainen, E. Lansimies, K. Bergstrom, and L. Niskanen Gender influence on vasoactive hormones at rest and during a 70{degrees} head-up tilt in healthy humans J Appl Physiol, April 1, 2002; 92(4): 1401 - 1408. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. A. Lipsitz Dynamics of Stability: The Physiologic Basis of Functional Health and Frailty J. Gerontol. A Biol. Sci. Med. Sci., March 1, 2002; 57(3): B115 - 125. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
 |
|
 T. P. Stein and C. E. Wade The catecholamine response to spaceflight: role of diet and gender Am J Physiol Endocrinol Metab, September 1, 2001; 281(3): E500 - E506. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. A. Ray Effect of gender on vestibular sympathoexcitation Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2000; 279(4): R1330 - R1333. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. S. Oberman, M. M. Gagnon, D. K. Kiely, J. C. Nelson, and L. A. Lipsitz Autonomic and Neurohumoral Control of Postprandial Blood Pressure in Healthy Aging J. Gerontol. A Biol. Sci. Med. Sci., August 1, 2000; 55(8): 477M - 483. [Abstract] [Full Text]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||