scholarly journals Orthostatic hypotension in aging humans

2000 ◽  
Vol 279 (4) ◽  
pp. H1548-H1554 ◽  
Author(s):  
Xiangrong Shi ◽  
D. Walter Wray ◽  
Kevin J. Formes ◽  
Hong-Wei Wang ◽  
Patrick M. Hayes ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Orthostatic Hypotension ◽  
Parasympathetic Nervous System ◽  
Lower Body Negative Pressure ◽  
The Elderly ◽  
Sympathetic Blockade ◽  
Lower Body ◽  
Younger Adults ◽  
Orthostatic Challenge

We tested the hypothesis that hypotension occurred in older adults at the onset of orthostatic challenge as a result of vagal dysfunction. Responses of heart rate (HR) and mean arterial pressure (MAP) were compared between 10 healthy older and younger adults during onset and sustained lower body negative pressure (LBNP). A younger group was also assessed after blockade of the parasympathetic nervous system with the use of atropine or glycopyrrolate and after blockade of the β1-adrenoceptor by use of metoprolol. Baseline HR (older vs. younger: 59 ± 4 vs. 54 ± 1 beats/min) and MAP (83 ± 2 vs. 89 ± 3 mmHg) were not significantly different between the groups. During −40 Torr, significant tachycardia occurred at the first HR response in the younger subjects without hypotension, whereas significant hypotension [change in MAP (ΔMAP) −7 ± 2 mmHg] was observed in the elderly without tachycardia. After the parasympathetic blockade, tachycardiac responses of younger subjects were diminished and associated with a significant hypotension at the onset of LBNP. However, MAP was not affected after the cardiac sympathetic blockade. We concluded that the elderly experienced orthostatic hypotension at the onset of orthostatic challenge because of a diminished HR response. However, an augmented vasoconstriction helped with the maintenance of their blood pressure during sustained LBNP.

Noise-Enhanced Heart Rate and Sympathetic Nerve Responses to Oscillatory Lower Body Negative Pressure in Humans

2001 ◽  
Vol 86 (2) ◽  
pp. 559-564 ◽  
Author(s):  
Ichiro Hidaka ◽  
Shin-Ichi Ando ◽  
Hideaki Shigematsu ◽  
Koji Sakai ◽  
Soko Setoguchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Stochastic Resonance ◽  
Negative Pressure ◽  
Sympathetic Nerve ◽  
Carotid Sinus ◽  
Lower Body Negative Pressure ◽  
Arterial System ◽  
Lower Body ◽  
Cardiopulmonary Baroreceptors

By injecting noise into the carotid sinus baroreceptors, we previously showed that heart rate (HR) responses to weak oscillatory tilt were enhanced via a mechanism known as “stochastic resonance.” It remains unclear, however, whether the same responses would be observed when using oscillatory lower body negative pressure (LBNP), which would unload the cardiopulmonary baroreceptors with physically negligible effects on the arterial system. Also, the vasomotor sympathetic activity directly controlling peripheral resistance against hypotensive stimuli was not observed. We therefore investigated the effects of weak (0 to approximately −10 mmHg) oscillatory (0.03 Hz) LBNP on HR and muscle sympathetic nerve activity (MSNA) while adding incremental noise to the carotid sinus baroreceptors via a pneumatic neck chamber. The signal-to-noise ratio of HR, cardiac interbeat interval, and total MSNA were all significantly improved by increasing noise intensity, while there was no significant change in the arterial blood pressure in synchronized with the oscillatory LBNP. We conclude that the stochastic resonance, affecting both HR and MSNA, results from the interaction of noise with the signal in the brain stem, where the neuronal inputs from the arterial and cardiopulmonary baroreceptors first come together in the nucleus tractus solitarius. Also, these results indicate that the noise could induce functional improvement in human blood pressure regulatory system in overcoming given hypotensive stimuli.

Differential sympathetic nerve and heart rate spectral effects of nonhypotensive lower body negative pressure

2001 ◽  
Vol 281 (2) ◽  
pp. R468-R475 ◽  
Author(s):  
John S. Floras ◽  
Gary C. Butler ◽  
Shin-Ichi Ando ◽  
Steven C. Brooks ◽  
Michael J. Pollard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Sympathetic Nerve ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Harmonic Component ◽  
Lower Body

Lower body negative pressure (LBNP; −5 and −15 mmHg) was applied to 14 men (mean age 44 yr) to test the hypothesis that reductions in preload without effect on stroke volume or blood pressure increase selectively muscle sympathetic nerve activity (MSNA), but not the ratio of low- to high-frequency harmonic component of spectral power (PL/PH), a coarse-graining power spectral estimate of sympathetic heart rate (HR) modulation. LBNP at −5 mmHg lowered central venous pressure and had no effect on stroke volume (Doppler) or systolic blood pressure but reduced vagal HR modulation. This latter finding, a manifestation of arterial baroreceptor unloading, refutes the concept that low levels of LBNP interrogate, selectively, cardiopulmonary reflexes. MSNA increased, whereas PL/PH and HR were unchanged. This discordance is consistent with selectivity of efferent sympathetic responses to nonhypotensive LBNP and with unloading of tonically active sympathoexcitatory atrial reflexes in some subjects. Hypotensive LBNP (−15 mmHg) increased MSNA and PL/PH, but there was no correlation between these changes within subjects. Therefore, HR variability has limited utility as an estimate of the magnitude of orthostatic changes in sympathetic discharge to muscle.

A genetic polymorphism of the α2-adrenergic receptor increases autonomic responses to stress

2004 ◽  
Vol 96 (6) ◽  
pp. 2231-2239 ◽  
Author(s):  
J. Clayton Finley ◽  
Michael O'Leary ◽  
Derin Wester ◽  
Steven MacKenzie ◽  
Neil Shepard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Individual Differences ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Gene Encoding ◽  
Autonomic Responses ◽  
Sweat Sodium

We hypothesized that individual differences in autonomic responses to psychological, physiological, or environmental stresses are inherited, and exaggerated autonomic responsiveness may represent an intermediate phenotype that can contribute to the development of essential hypertension in humans over time. α2-Adrenergic receptors (α2-ARs), encoded by a gene on chromosome 10, are found in the central nervous system and also mediate release of norepinephrine from the presynaptic nerve terminals of the peripheral sympathetic nervous system and the exocytosis of epinephrine from the adrenal medulla. We postulated that, because this receptor mediates central and peripheral autonomic responsiveness to stress, genetic mutations in the gene encoding this receptor may explain contrasting activity of the autonomic nervous system among individuals. The restriction enzyme Dra I identifies a polymorphic site in the 3′-transcribed, but not translated, portion of the gene encoding the chromosome 10 α2-AR. Southern blotting of genomic DNA with a cDNA probe after restriction enzyme digestion results in fragments that are either 6.7 kb or 6.3 kb in size. Transfection studies of these two genotypes resulted in contrasting expression of a reporter gene, and it is suggested from these findings that this is a functional polymorphism. In a study of 194 healthy subjects, we measured autonomic responses to provocative motion, a fall in blood pressure induced by decreasing venous return and cardiac output, or exercise. Specifically, we measured reactions to 1) Coriolis stress, a strong stimulus that induces motion sickness in man; 2) heart rate responses to the fall in blood pressure induced by the application of graded lower body negative pressure; and 3) exercise-induced sweat secretion. In all of these paradigms of stress, subjective and objective evidence of increased autonomic responsiveness was found in those individuals harboring the 6.3-kb allele. Specifically, volunteers with the 6.3-kb allele had greater signs and symptoms of motion sickness mediated by the autonomic nervous system after off-axis rotation at increasing velocity (number of head movements a subject could complete during rotation before emesis ± SE: 295 ± 18 vs. 365 ± 11; P = 0.001). They also had greater increases in heart rate in responses to the lower body negative pressure-induced fall in blood pressure (increase in heart rate ± SE: 3.0 ± 0.4 vs. 1.8 ± 0.3; P = 0.012), and the 6.3-kb group had higher sweat sodium concentrations during exercise (mean sweat sodium concentration in meq/l over 30 min of exercise ± SE: 43.2 ± 7.1 vs. 27.6 ± 3.4; P < 0.05). This single-nucleotide polymorphism may contribute to contrasting individual differences in autonomic responsiveness among healthy individuals.

Hemodynamic Strategies in Blood Pressure Regulation During Orthostatic Challenge in Women

1997 ◽  
Vol 22 (4) ◽  
pp. 351-367
Author(s):  
Tania L. Culham ◽  
Gabrielle K. Savard
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
Orthostatic Challenge ◽  
Carotid Baroreflex

Several studies indicate that carotid baroreflex responsiveness is a good predictor of orthostatic tolerance. Two groups of healthy women with high (HI) and low (LO) carotid baroreflex responsiveness were studied (a) to determine any differences in the level of orthostatic tolerance of the two groups, and (b) to study the hemodynamic strategies used by HI and LO responders to regulate arterial pressure during the orthostatic challenge of lower body negative pressure (LBNP). Orthostatic tolerance was similar between the two groups, whereas the hemodynamic strategies recruited to maintain blood pressure at −40 mmHg LBNP differed: HI responders exhibited greater LBNP-induced decreases in stroke volume and cardiac output, as well as a greater increase in peripheral resistance compared to LO responders (p < .05). In addition, a significant increase in plasma renin activity during LBNP was found in the HI responders only. No significant between-group differences were found in arterial and cardiopulmonary control of vascular resistance or arterial haroreflex control of heart rate during LBNP. Key words: arterial pressure, carotid baroreceptor, lower body negative pressure, orthostatic tolerance, stroke volume

Carotid arterial haemodynamics after mild degrees of lower-body negative pressure in man

1992 ◽  
Vol 83 (5) ◽  
pp. 535-540 ◽  
Author(s):  
P. J. Lacolley ◽  
B. M. Pannier ◽  
M. A. Slama ◽  
J. L. Cuche ◽  
A. P. G. Hoeks ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Weight Bearing ◽  
Normal Subjects ◽  
Lower Body ◽  
Head Up Tilt ◽  
Cardiopulmonary Receptors ◽  
Carotid Arterial

1. Pulsatile changes in the diameter of the common carotid artery were studied transcutaneously using an echo-tracking technique in 15 normal subjects: eight subjects before and during application of graded lower-body negative pressure from −5 to −15 mmHg, and seven subjects before and during weight-bearing head-up tilt at 30 and 60 degrees. 2. In concomitant studies of changes in forearm vascular resistance, it was seen that mild lower-body negative pressure produced deactivation of cardiopulmonary receptors without changes in systemic blood pressure or heart rate. 3. After lower-body negative pressure, a significant decrease in carotid arterial diastolic diameter [from 0.662 ± 0.028 to 0.624 ± 0.033 cm (lower-body negative pressure −10 mmHg) and 0.640 ± 0.030 cm lower-body negative pressure −15 mmHg), P<0.001 and <0.05] was observed. 4. After head-up tilt, carotid arterial diameter was also significantly decreased at 30 and 60 degrees, whereas a significant increase in heart rate occurred only at 60 degrees and mean blood pressure did not change. 5. The study provides evidence that the geometry of the arterial wall is substantially modified by noninvasive manoeuvres such as head-up tilting and lower-body negative pressure. The latter is assumed to selectively deactivate human cardiopulmonary receptors, but the present data suggest that local changes may also influence carotid baroreceptors.

scholarly journals Validity of auscultatory and Penaz blood pressure measurements during profound heat stress alone and with an orthostatic challenge

2011 ◽  
Vol 301 (5) ◽  
pp. R1510-R1516 ◽  
Author(s):  
Matthew S. Ganio ◽  
R. Matthew Brothers ◽  
Rebekah A. I. Lucas ◽  
Jeffrey L. Hastings ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Heat Stress ◽  
Brachial Artery ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Pressure Measurements ◽  
Lower Body ◽  
Dynamic Changes ◽  
Orthostatic Challenge

Despite frequent reporting of blood pressure (BP) during profound passive heat stress, both with and without a hypotensive challenge, the method by which BP is measured often varies between laboratories. It is unknown whether auscultatory and finger BP measures accurately reflect intra-arterial BP during dynamic changes in cardiac output and peripheral resistance associated with the aforementioned conditions. The purpose of this investigation was to test the hypothesis that auscultatory BP measured at the brachial artery, and finger BP measured by the Penaz method, are valid measures of intra-arterial BP during a passive heat stress and a heat-stressed orthostatic challenge, via lower body negative pressure (LBNP). Absolute (specific aim 1) and the change in (specific aim 2) systolic (SBP), diastolic (DBP), and mean BPs (MBP) were compared at normothermia, after a core temperature increase of 1.47 ± 0.09°C, and during subsequent LBNP. Heat stress did not change auscultatory SBP (6 ± 11 mmHg; P = 0.16), but Penaz SBP (−22 ± 16 mmHg; P < 0.001) and intra-arterial SBP (−11 ± 13 mmHg P = 0.017) decreased. In contrast, DBP and MBP did not differ between methods throughout heat stress. Compared with BP before LBNP, the magnitude of the reduction in BP with all three methods was similar throughout LBNP ( P > 0.05). In conclusion, auscultatory SBP and Penaz SBP failed to track the decrease in intra-arterial SBP that occurred during the profound heat stress, while decreases in arterial BP during an orthostatic challenge are comparable between methodologies.

scholarly journals Insufficient cutaneous vasoconstriction leading up to and during syncopal symptoms in the heat stressed human

2010 ◽  
Vol 299 (4) ◽  
pp. H1168-H1173 ◽  
Author(s):  
C. G. Crandall ◽  
M. Shibasaki ◽  
T. E. Wilson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Internal Temperature ◽  
Orthostatic Challenge ◽  
Head Up Tilt ◽  
Cutaneous Vasoconstriction

As much as 50% of cardiac output can be distributed to the skin in the hyperthermic human, and therefore the control of cutaneous vascular conductance (CVC) becomes critical for the maintenance of blood pressure. Little is known regarding the magnitude of cutaneous vasoconstriction in profoundly hypotensive individuals while heat stressed. This project investigated the hypothesis that leading up to and during syncopal symptoms associated with combined heat and orthostatic stress, reductions in CVC are inadequate to prevent syncope. Using a retrospective study design, we evaluated data from subjects who experienced syncopal symptoms during lower body negative pressure ( N = 41) and head-up tilt ( N = 5). Subjects were instrumented for measures of internal temperature, forearm skin blood flow, arterial pressure, and heart rate. CVC was calculated as skin blood flow/mean arterial pressure × 100. Data were obtained while subjects were normothermic, immediately before an orthostatic challenge while heat stressed, and at 5-s averages for the 2 min preceding the cessation of the orthostatic challenge due to syncopal symptoms. Whole body heat stress increased internal temperature (1.25 ± 0.3°C; P < 0.001) and CVC (29 ± 20 to 160 ± 58 CVC units; P < 0.001) without altering mean arterial pressure (83 ± 7 to 82 ± 6 mmHg). Mean arterial pressure was reduced to 57 ± 9 mmHg ( P < 0.001) immediately before the termination of the orthostatic challenge. At test termination, CVC decreased to 138 ± 61 CVC units ( P < 0.001) relative to before the orthostatic challenge but remained approximately fourfold greater than when subjects were normothermic. This negligible reduction in CVC during pronounced hypotension likely contributes to reduced orthostatic tolerance in heat-stressed humans. Given that lower body negative pressure and head-up tilt are models of acute hemorrhage, these findings have important implications with respect to mechanisms of compromised blood pressure control in the hemorrhagic individual who is also hyperthermic (e.g., military personnel, firefighters, etc.).

scholarly journals Sex differences in cardiovascular responses to orthostatic challenge in healthy older persons: A pilot study

2019 ◽  
Vol 106 (3) ◽  
pp. 236-249 ◽  
Author(s):  
C Sachse ◽  
I Trozic ◽  
B Brix ◽  
A Roessler ◽  
N Goswami
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Sex Differences ◽  
Orthostatic Hypotension ◽  
Older Persons ◽  
Cardiovascular Responses ◽  
Parasympathetic Activity ◽  
Hemodynamic Parameters ◽  
Orthostatic Challenge

Background Premenopausal women show a higher incidence of orthostatic hypotension than age-matched men, but there are limited data available on sex differences in cardiovascular responses to orthostatic challenge in healthy older persons. We investigated sex differences in hemodynamic and autonomic responses to orthostatic challenge in healthy older males and females. Materials and methods Fourteen older healthy women and 10 age-matched men performed a sit-to-stand test (5 min of sitting followed by 5 min of standing). A Task Force® Monitor continuously measured the following beat-to-beat hemodynamic parameters: heart rate, systolic blood pressure, diastolic blood pressure, mean blood pressure, stroke index, cardiac index, and total peripheral resistance index. Cardiac autonomic activity, low-frequency (LF: 0.04–0.15 Hz) normalized (LFnuRRI) and high-frequency (HF: 0.15–0.4 Hz) normalized (HFnuRRI) components, and the ratio between LF and HF power (LF/HF) were calculated using power spectral analysis of heart rate variability. Results Across all hemodynamic parameters, there were no significant differences between the sexes at baseline and during standing. LFnuRRI (median: 70.2 vs. 52.3, p < 0.05) and LF/HF ratio (median: 2.4 vs. 1.1, p < 0.05) were significantly higher, whereas HFnuRRI (median: 29.8 vs. 47.7, p < 0.05) was lower among women at baseline. All other heart rate variability measures did not differ between the sexes. Conclusions The data indicate that older women showed higher sympathetic and lower parasympathetic activity at rest compared to age-matched men. These results are contradictory to the observations from previous studies, which showed a reduced sympathetic and enhanced parasympathetic activity in women in all ages. Further studies are required to determine the underlying mechanisms contributing to higher incidence of orthostatic hypotension in older females.

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