The Effect of Mental Arithmetic on Blood Pressure Variability and Baroreflex Sensitivity in Man

1978 ◽  
Vol 55 (s4) ◽  
pp. 381s-382s ◽  
Author(s):  
P. Sleight ◽  
P. Fox ◽  
R. Lopez ◽  
D. E. Brooks

1. Baroreflex sensitivity was tested in three normal, three borderline and one hypertensive subject before and during mental arithmetic, the prolongation of pulse interval caused by a provoked rise in blood pressure being used as a measure of baroreflex sensitivity. 2. Baroreflex sensitivity was significantly decreased during mental arithmetic. 3. During mental arithmetic the arterial pressure fluctuated markedly. 4. These findings suggest that in man, as well as animals, the defence of alerting reaction depresses baroreflex control and thus contributes to the rise in blood pressure seen at this time.

1995 ◽  
Vol 268 (4) ◽  
pp. H1606-H1612 ◽  
Author(s):  
G. Parati ◽  
A. Frattola ◽  
M. Di Rienzo ◽  
P. Castiglioni ◽  
A. Pedotti ◽  
...  

The effects of aging on the dynamic modulation of baroreflex sensitivity over 24 h was assessed in eight elderly (mean age +/- SD, 63.9 +/- 3.2 yr) and in eight young (23.9 +/- 6.1 yr) mild or moderate essential hypertensive patients, who were subject to a 24-h intra-arterial (Oxford technique) blood pressure recording in ambulatory conditions. The sensitivity of baroreflex control of the heart rate was dynamically assessed by quantifying 1) the slope of the regression line between pulse interval (the reciprocal of heart rate) and systolic blood pressure changes over spontaneously occurring hypertension-bradycardia or hypotension-tachycardia sequences (time domain analysis) and 2) the ratio between spectral-powers of pulse interval and systolic blood pressure around 0.1 Hz (alpha-coefficient: frequency domain analysis). The 24-h average sequence slope was lower in old than in young individuals (4.4 +/- 0.5 vs. 9.9 +/- 1.3 and 4.8 +/- 0.7 vs. 8.4 +/- 1.4 ms/mmHg for hypertension-bradycardia and hypotension-tachycardia sequences, respectively; P < 0.05 for both). Similar results were obtained by using the alpha-coefficient approach. The marked nighttime increase in baroreflex sensitivity observed in young individuals was much less evident in the elderly. Thus 24-h baroreflex sensitivity is markedly impaired by aging. The impairment becomes manifest also as an inability to increase baroreflex sensitivity at night.


1979 ◽  
Vol 57 (s5) ◽  
pp. 169s-171s ◽  
Author(s):  
P. Sleight ◽  
J. S. Floras ◽  
M. O. Hassan ◽  
J. V. Jones ◽  
B. A. Osikowska ◽  
...  

1. Twelve subjects (mean age 46·3 ± 12·5 years) with mild to moderate hypertension were studied before, during and after bicycle ergometer exercise. 2. Baroreflex sensitivity was determined by the Oxford phenylephrine method; sensitivity at rest was inversely related to intra-arterial pressure and age. Age and resting arterial pressure were not related. 3. Exercise for 5 min at 50 W and 5 min at 75 W raised the mean arterial pressure from 116·4 ± 18·0 to 150·0 ± 25·4 mmHg, the heart rate from 73·2 to 126·7 beats/min and the plasma noradrenaline from 541 ± 142·7 to 1309·8 ± 543·5 pg/ml (P &lt; 0·001). 4. The increase in noradrenaline during exercise and the maximum mean pressure achieved were inversely related to resting baroreflex sensitivity (r = −0·68 and −0·77 respectively). Resting values of noradrenaline were not related to baroreflex sensitivity, age, or resting blood pressure. 5. It is possible that the rise in both plasma noradrenaline and arterial blood pressure produced by exercise is controlled by the baroreceptor reflexes; these are less effective in hypertensive subjects and thus the increases in noradrenaline and arterial pressure during exercise are greater in subjects with raised blood pressure.


2003 ◽  
Vol 95 (5) ◽  
pp. 1789-1798 ◽  
Author(s):  
Kichang Lee ◽  
Dwayne N. Jackson ◽  
Douglas L. Cordero ◽  
Takeshi Nishiyasu ◽  
Jochen K. Peters ◽  
...  

Spontaneous baroreflex control of pulse interval (PI) was assessed in healthy volunteers under thermoneutral and heat stress conditions. Subjects rested in the supine position with their lower legs in a water bath at 34°C. Heat stress was imposed by increasing the bath temperature to 44°C. Arterial blood pressure (Finapres), PI (ECG), esophageal and skin temperature, and stroke volume were continuously collected during each 5-min experimental stage. Spontaneous baroreflex function was evaluated by multiple techniques, including 1) the mean slope of the linear relationship between PI and systolic blood pressure (SBP) with three or more simultaneous increasing or decreasing sequences, 2) the linear relationship between changes in PI and SBP (ΔPI/ΔSBP) derived by using the first differential equation, 3) the linear relationship between changes in PI and SBP with simultaneously increasing or decreasing sequences (+ΔPI/+ΔSBP or -ΔPI/-ΔSBP), and 4) transfer function analysis. Heat stress increased esophageal temperature by 0.6 ± 0.1°C, decreased PI from 1,007 ± 43 to 776 ± 37 ms and stroke volume by 16 ± 5 ml/beat. Heat stress reduced baroreflex sensitivity but increased the incidence of baroreflex slopes from 5.2 ± 0.8 to 8.6 ± 0.9 sequences per 100 heartbeats. Baroreflex sensitivity was significantly correlated with PI or vagal power ( r2 = 0.45, r2 = 0.71, respectively; P < 0.05). However, the attenuation in baroreflex sensitivity during heat stress appeared related to a shift in autonomic balance (shift in resting PI) rather than heat stress per se.


1995 ◽  
Vol 88 (1) ◽  
pp. 103-109 ◽  
Author(s):  
Peter Sleight ◽  
Maria Teresa La Rovere ◽  
Andrea Mortara ◽  
Gianni Pinna ◽  
Roberto Maestri ◽  
...  

1. It is often assumed that the power in the low-(around 0.10 Hz) and high-frequency (around 0.25 Hz) bands obtained by power spectral analysis of cardiovascular variables reflects vagal and sympathetic tone respectively. An alternative model attributes the low-frequency band to a resonance in the control system that is produced by the inefficiently slow time constant of the reflex response to beat-to-beat changes in blood pressure effected by the sympathetic (with or without the parasympathetic) arm(s) of the baroreflex (De Boer model). 2. We have applied the De Boer model of circulatory variability to patients with varying baroreflex sensitivity and one normal subject, and have shown that the main differences in spectral power (for both low and high frequency) between and within subjects are caused by changes in the arterial baroreflex gain, particularly for vagal control of heart rate (R—R interval) and left ventricular stroke output. We have computed the power spectrum at rest and during neck suction (to stimulate carotid baroreceptors). We stimulated the baroreceptors at two frequencies (0.1 and 0.2 Hz), which were both distinct from the controlled respiration rate (0.25 Hz), in both normal subjects and heart failure patients with either sensitive or poor baroreflex control. 3. The data broadly confirm the De Boer model. The low-frequency (0.1 Hz) peak in either R—R or blood pressure variability) was spontaneously generated only if the baroreflex control of the autonomic outflow was relatively intact. With a large stimulus to the carotid baroreceptor it was possible to influence the low-frequency R—R but not low-frequency blood pressure variability. This implies that it is too simplistic to use power spectral analysis as a simple measure of autonomic balance its underlying modulation is more complex than generally believed. 4. It may be that power spectral analysis is more a sensitive indicator of baroreflex control, particularly of vagal control, than direct evidence of autonomic balance. of course, there is often a correlation between the gain of the reflex and the autonomic balance of vagus and sympathetic. These considerations may help our understanding of some conditions, such as exercise or heart failure, when the power spectral analysis method fails to identify increased sympathetic discharge; this failure may partly be explained by the decrease in baroreflex sensitivity which occurs in these two conditions.


1980 ◽  
Vol 59 (s6) ◽  
pp. 401s-404s ◽  
Author(s):  
G. Mancia ◽  
A. Ferrari ◽  
L. Gregorini ◽  
G. Parati ◽  
G. Pomidossi ◽  
...  

1. Intra-arterial blood pressure and heart rate were recorded for 24 h in ambulant hospitalized patients of variable age who had normal blood pressure or essential hypertension. Mean 24 h values, standard deviations and variation coefficient were obtained as the averages of values separately analysed for 48 consecutive half-hour periods. 2. In older subjects standard deviation and variation coefficient for mean arterial pressure were greater than in younger subjects with similar pressure values, whereas standard deviation and variation coefficient for heart rate were smaller. 3. In hypertensive subjects standard deviation for mean arterial pressure was greater than in normotensive subjects of similar ages, but this was not the case for variation coefficient, which was slightly smaller in the former than in the latter group. Normotensive and hypertensive subjects showed no difference in standard deviation and variation coefficient for heart rate. 4. In both normotensive and hypertensive subjects standard deviation and even more so variation coefficient were slightly or not related to arterial baroreflex sensitivity as measured by various methods (phenylephrine, neck suction etc.). 5. It is concluded that blood pressure variability increases and heart rate variability decreases with age, but that changes in variability are not so obvious in hypertension. Also, differences in variability among subjects are only marginally explained by differences in baroreflex function.


2005 ◽  
Vol 20 (4) ◽  
pp. 394 ◽  
Author(s):  
V. Papaioannou ◽  
M. Giannakou ◽  
N. Maglaveras ◽  
E. Sofianos ◽  
M. Giala

2008 ◽  
Vol 295 (3) ◽  
pp. H1150-H1155 ◽  
Author(s):  
François Cottin ◽  
Claire Médigue ◽  
Yves Papelier

The aim of the study was to assess the instantaneous spectral components of heart rate variability (HRV) and systolic blood pressure variability (SBPV) and determine the low-frequency (LF) and high-frequency baroreflex sensitivity (HF-BRS) during a graded maximal exercise test. The first hypothesis was that the hyperpnea elicited by heavy exercise could entail a significant increase in HF-SBPV by mechanical effect once the first and second ventilatory thresholds (VTs) were exceeded. It was secondly hypothesized that vagal tone progressively withdrawing with increasing load, HF-BRS could decrease during the exercise test. Fifteen well-trained subjects participated in this study. Electrocardiogram (ECG), blood pressure, and gas exchanges were recorded during a cycloergometer test. Ventilatory equivalents were computed from gas exchange parameters to assess VTs. Spectral analysis was applied on cardiovascular series to compute RR and systolic blood pressure power spectral densities, cross-spectral coherence, gain, and α index of BRS. Three exercise intensity stages were compared: below (A1), between (A2), and above (A3) VTs. From A1 to A3, both HF-SBPV (A1: 45 ± 6, A2: 65 ± 10, and A3: 120 ± 23 mm2Hg, P < 0.001) and HF-HRV increased (A1: 20 ± 5, A2: 23 ± 8, and A3:40 ± 11 ms2, P < 0.02), maintaining HF-BRS (gain, A1: 0.68 ± 0.12, A2: 0.63 ± 0.08, and A3: 0.57 ± 0.09; α index, A1: 0.58 ± 0.08, A2: 0.48 ± 0.06, and A3: 0.50 ± 0.09 ms/mmHg, not significant). However, LF-BRS decreased (gain, A1: 0.39 ± 0.06, A2: 0.17 ± 0.02, and A3: 0.11 ± 0.01, P < 0.001; α index, A1: 0.46 ± 0.07, A2: 0.20 ± 0.02, and A3: 0.14 ± 0.01 ms/mmHg, P < 0.001). As expected, once VTs were exceeded, hyperpnea induced a marked increase in both HF-HRV and HF-SBPV. However, this concomitant increase allowed the maintenance of HF-BRS, presumably by a mechanoelectric feedback mechanism.


Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 727-727
Author(s):  
Ovidiu Baltatu ◽  
Ben J Janssen ◽  
Ralph Plehm ◽  
Detlev Ganten ◽  
Michael Bader

P191 The brain renin-angiotensin system (RAS) system may play a functional role in the long-term and short-term control of blood pressure (BPV) and heart rate variability (HRV). To study this we recorded in transgenic rats TGR(ASrAOGEN) with low brain angiotensinogen levels the 24-h variation of BP and HR during basal and hypertensive conditions, induced by a low-dose s.c. infusion of angiotensin II (Ang II, 100 ng/kg/min) for 7 days. Cardiovascular parameters were monitored by telemetry. Short-term BPV and HRV were evaluated by spectral analysis and as a measure of baroreflex sensitivity the transfer gain between the pressure and heart rate variations was calculated. During the Ang II infusion, in SD but not TGR(ASrAOGEN) rats, the 24-h rhythm of BP was inverted (5.8 ± 2 vs. -0.4 ± 1.8 mm Hg/group of day-night differences of BP, p< 0.05, respectively). In contrast, in both the SD and TGR(ASrAOGEN) rats, the 24-h HR rhythms remained unaltered and paralleled those of locomotor activity. The increase of systolic BP was significantly reduced in TGR(ASrAOGEN) in comparison to SD rats as previously described, while the HR was not altered in TGR(ASrAOGEN) nor in SD rats. The spectral index of baroreflex sensitivity (FFT gain between 0.3-0.6 Hz) was significantly higher in TGR(ASrAOGEN) than SD rats during control (0.71 ± 0.1 vs. 0.35 ± 0.06, p<0.05), but not during Ang II infusion (0.6 ± 0.07 vs. 0.4 ± 0.1, p>0.05). These results demonstrate that the brain RAS plays an important role in mediating the effects of Ang II on the circadian variation of BP. Furthermore these data are consistent with the view that the brain RAS modulates baroreflex control of HR in rats, with AII having an inhibitory role.


Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Kátia B Scapini ◽  
Valéria C Hong ◽  
Janaína B Ferreira ◽  
Sílvia B Souza ◽  
Naomi V Ferreira ◽  
...  

Background: Patients with end-stage renal disease (ESRD) undergoing hemodialysis are susceptible to the development of autonomic dysfunction, which is associated with an increased risk of sudden death. Experimental and clinical evidence suggest a crucial role of autonomic dysfunction for both, the progression of renal disease and for the high rate of cardiovascular events in these patients. In the present study, we evaluated the heart rate variability (HRV), the blood pressure variability (BPV) and the baroreflex sensitivity (BRS) in ESRD patients undergoing hemodialysis and normal controls. Methods: Nine ESRD patients undergoing hemodialysis (mean age 53.4±10.2 years, 4 male) and nine age-matched healthy controls (mean age 52.8±10.2 years, 4 male) were assessed. Non−invasive curves of blood pressure (BP) were recorded continuously (Finometer ®) for 10 minutes, at rest, in the supine position. The heart rate variability (HRV) and systolic blood pressure variability (BPV) were estimated in the time and frequency domain (spectral analysis). The BRS was quantified by alpha index. Statistical analyzes were performed by Student's t test and the results were expressed as mean ± standard deviation. Results: ESRD patients presented lower HRV in time domain than healthy controls (SDNN: 25.8±10.7 vs. 44.6±11.7 ms, p<0.01; VAR NN: 768.3±607.4 vs. 2113.9±1261.6 ms 2 , p=0.01). All frequency domain analyzed indexes, i.e., total power (361.9±297.0 vs. 1227.2±696.3 ms 2 , p<0.01), high-frequency (181.8±128.7 vs. 358.7±179.8 ms 2 , p=0.047), low-frequency (55.1±44.2 vs. 444.6±389.9 ms 2 , p=0.02) and very-low-frequency (72.5±75.1 vs. 279.2±119.5 ms 2 , p<0.01) of HRV were lower in ESRD patients. The BPV was higher in ESRD patients when compared to controls (VAR PAS: 98.4±72.0 vs. 35.4±21.4 ms 2 , p=0.03) and BRS was lower in ESRD patients (alpha index: 4.34±3.05 vs. 7.56±2.50 ms/mmHg, p<0.02). Conclusion: ESRD patients undergoing hemodialysis presents reduced HRV, increase in BPV and reduced baroreflex sensitivity. These impairments may be associated with mortality in ESRD.


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