Circulatory responses to lower body negative pressure in young Afghans and Danes: implications for understanding ethnic effects on blood pressure regulation

2014 ◽  
Vol 114 (11) ◽  
pp. 2321-2329
Author(s):  
Ali Asmar ◽  
Jens Bülow ◽  
Lene Simonsen ◽  
Jonas G. Rasmussen ◽  
Niels J. Christensen ◽  
...  
2001 ◽  
Vol 86 (2) ◽  
pp. 559-564 ◽  
Author(s):  
Ichiro Hidaka ◽  
Shin-Ichi Ando ◽  
Hideaki Shigematsu ◽  
Koji Sakai ◽  
Soko Setoguchi ◽  
...  

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.


2001 ◽  
Vol 281 (2) ◽  
pp. R468-R475 ◽  
Author(s):  
John S. Floras ◽  
Gary C. Butler ◽  
Shin-Ichi Ando ◽  
Steven C. Brooks ◽  
Michael J. Pollard ◽  
...  

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.


1997 ◽  
Vol 22 (4) ◽  
pp. 351-367
Author(s):  
Tania L. Culham ◽  
Gabrielle K. Savard

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


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 ◽  
...  

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.


1993 ◽  
Vol 75 (5) ◽  
pp. 1984-1988 ◽  
Author(s):  
A. T. Hirsch ◽  
J. A. Majzoub ◽  
C. J. Ren ◽  
K. M. Scales ◽  
M. A. Creager

In animals subjected to hemorrhage, plasma arginine vasopressin concentrations increase to levels sufficient to cause vasoconstriction, thus attenuating the hypotensive response. The purpose of this study was to examine the contribution of vasopressin to blood pressure regulation during hypotension in humans. Hypotension was induced in twelve normal subjects by lower body negative pressure (LBNP) before and after intravenous administration of vasopressin V1 receptor antagonist. Before drug administration, LBNP reduced systolic blood pressure from 125 +/- 4 to 78 +/- 12 mmHg (P < 0.01) as vasopressin concentration increased from 2.9 +/- 0.6 to 17 +/- 6 pg/ml (P < 0.05). After administration of the vasopressin antagonist, LBNP reduced systolic blood pressure from 128 +/- 3 to 89 +/- 11 mmHg (P < 0.01). The hypotensive response to LBNP was not potentiated by inhibiting vasopressin's vasoconstrictive effects (P = NS). Thus hypotension causes marked increases in plasma vasopressin concentration. In contrast to findings in animal studies, however, vasopressin does not contribute to the maintenance of blood pressure during hypotension in humans.


2001 ◽  
Vol 280 (4) ◽  
pp. R947-R958 ◽  
Author(s):  
Victor A. Convertino

The purpose of this study was to test the hypothesis that repeated exposure to high acceleration (G) would be associated with enhanced functions of specific mechanisms of blood pressure regulation. We measured heart rate (HR), stroke volume (SV), cardiac output (Q̊), mean arterial blood pressure, central venous pressure, forearm and leg vascular resistance, catecholamines, and changes in leg volume (%ΔLV) during various protocols of lower body negative pressure (LBNP), carotid stimulation, and infusions of adrenoreceptor agonists in 10 males after three training sessions on different days over a period of 5–7 days using a human centrifuge (G trained). These responses were compared with the same measurements in 10 males who were matched for height, weight, and fitness but did not undergo G training (controls). Compared with the control group, G-trained subjects demonstrated greater R-R interval response to equal carotid baroreceptor stimulation (7.3 ± 1.2 vs. 3.9 ± 0.4 ms/mmHg, P = 0.02), less vasoconstriction to equal low-pressure baroreceptor stimulation (−1.4 ± 0.2 vs. −2.6 ± 0.3 U/mmHg, P = 0.01), and higher HR (−1.2 ± 0.2 vs. −0.5 ± 0.1 beats · min−1 · mmHg−1, P = 0.01) and α-adrenoreceptor response (32.8 ± 3.4 vs. 19.5 ± 4.7 U/mmHg, P = 0.04) to equal dose of phenylephrine. During graded LBNP, G-trained subjects had less decline in Q̊ and SV, %ΔLV, and elevation in thoracic impedance. G-trained subjects also had greater total blood (6,497 ± 496 vs. 5,438 ± 228 ml, P = 0.07) and erythrocyte (3,110 ± 364 vs. 2,310 ± 96 ml, P = 0.06) volumes. These results support the hypothesis that exposure to repeated high G is associated with increased capacities of mechanisms that underlie blood pressure regulation.


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