Baroreflex Control of Blood Pressure and Plasma Noradrenaline during Exericse in Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 169s-171s ◽  
Author(s):  
P. Sleight ◽  
J. S. Floras ◽  
M. O. Hassan ◽  
J. V. Jones ◽  
B. A. Osikowska ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Bicycle Ergometer ◽  
Plasma Noradrenaline ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Ergometer Exercise ◽  
Resting Blood Pressure ◽  
Mean Pressure

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 < 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.

Thyroid status influences baroreflex function and autonomic contributions to arterial pressure and heart rate

2001 ◽  
Vol 280 (5) ◽  
pp. H2061-H2068 ◽  
Author(s):  
C. Michael Foley ◽  
Richard M. McAllister ◽  
Eileen M. Hasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Logistic Function ◽  
Arterial Baroreflex ◽  
Thyroid Status ◽  
Baroreflex Control ◽  
Baroreflex Function ◽  
Resting Blood Pressure ◽  
Sympathetic Influence

The effect of thyroid status on arterial baroreflex function and autonomic contributions to resting blood pressure and heart rate (HR) were evaluated in conscious rats. Rats were rendered hyperthyroid (Hyper) or hypothyroid (Hypo) with triiodothyronine and propylthiouracil treatments, respectively. Euthyroid (Eut), Hyper, and Hypo rats were chronically instrumented to measure mean arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). Baroreflex function was evaluated with the use of a logistic function that relates LSNA or HR to MAP during infusion of phenylephrine and sodium nitroprusside. Contributions of the autonomic nervous system to resting MAP and HR were assessed by blocking autonomic outflow with trimethaphan. In Hypo rats, the arterial baroreflex curve for both LSNA and HR was shifted downward. Hypo animals exhibited blunted sympathoexcitatory and tachycardic responses to decreases in MAP. Furthermore, the data suggest that in Hypo rats, the sympathetic influence on HR was predominant and the autonomic contribution to resting MAP was greater than in Eut rats. In Hyper rats, arterial baroreflex function generally was similar to that in Eut rats. The autonomic contribution to resting MAP was not different between Hyper and Eut rats, but predominant parasympathetic influence on HR was exhibited in Hyper rats. The results demonstrate baroreflex control of LSNA and HR is attenuated in Hypo but not Hyper rats. Thyroid status alters the balance of sympathetic to parasympathetic tone in the heart, and the Hypo state increases the autonomic contributions to resting blood pressure.

Relating drug-induced changes in carotid artery mechanics to cardiovagal and sympathetic baroreflex control

2005 ◽  
Vol 83 (5) ◽  
pp. 439-446 ◽  
Author(s):  
Deborah D O'Leary ◽  
Craig D Steinback ◽  
Angela D Cechetto ◽  
Blaine T Foell ◽  
Jane C Topolovec ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Baroreflex Sensitivity ◽  
Muscle Sympathetic Nerve Activity ◽  
Pressure Change ◽  
Drug Induced ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Induced Changes

Previous evidence indicates that sensitivity of the baroreflex cardiovagal and sympathetic arms is dissociated. In addition, pharmacologic assessment of baroreflex sensitivity (BRS) has revealed that cardiovagal, but not sympathetic, BRS is greater when blood pressure is increasing versus falling. The origin of this hysteresis is unknown. In this study, carotid artery distensibility and absolute distension (diameter) were assessed to test the hypothesis that vessel mechanics in barosensitive regions affect the BRS of cardiovagal, but not sympathetic, outflow. R-R interval (i.e. time between successive R waves), finger arterial blood pressure, muscle sympathetic nerve activity, and carotid artery dimensions (B-mode imaging) were measured during sequential infusions of sodium nitroprusside (SNP) and phenylephrine (PHE). Systolic and diastolic common carotid artery diameters and pulse pressure were recorded to calculate distensibility of this vessel under each drug condition. Cardiovagal BRS was greater when blood pressure was increasing versus decreasing (p < 0.01). Sympathetic BRS was not affected by direction of pressure change. Distensibility did not differ between SNP and PHE injections. However, compared with SNP, infusion of PHE resulted in larger absolute systolic and diastolic carotid diameters (p < 0.001). Therefore, cardiovagal reflex hysteresis was related to drug-induced changes in common carotid artery diameter but not distensibility. The lack of sympathetic hysteresis in this model suggests a relative insensitivity of this baroreflex component to carotid artery dimensions and provides a possible mechanism for the dissociation between cardiovagal and sympathetic BRS.Key words: Oxford method, baroreflex hysteresis, cardiovagal, MSNA, distensibility.

Role of the area postrema in angiotensin II modulation of baroreflex control of heart rate in conscious mice

2003 ◽  
Vol 284 (3) ◽  
pp. H1003-H1007 ◽  
Author(s):  
Baojian Xue ◽  
Hope Gole ◽  
Jaya Pamidimukkala ◽  
Meredith Hay
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Area Postrema ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Intravenous Infusions

This study reports the effects of angiotensin II (ANG II), arginine vasopression (AVP), phenylephrine (PE), and sodium nitroprusside (SNP) on baroreflex control of heart rate in the presence and absence of the area postrema (AP) in conscious mice. In intact, sham-lesioned mice, baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of ANG II were significantly less than those observed with similar increases in arterial pressure with PE (slope: −3.0 ± 0.9 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). Baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of AVP were the same as those observed with PE in sham animals (slope: −5.8 ± 0.7 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). After the AP was lesioned, the slope of baroreflex inhibition of heart rate was the same whether pressure was increased with ANG II, AVP, or PE. The slope of the baroreflex-induced increases in heart rate due to decreases in arterial blood pressure with SNP were the same in sham- and AP-lesioned animals. These results indicate that, similar to other species, in mice the ability of ANG II to acutely reset baroreflex control of heart rate is dependent on an intact AP.

NTS neuronal responses to arterial pressure and pressure changes in the rat

1993 ◽  
Vol 265 (6) ◽  
pp. R1355-R1368 ◽  
Author(s):  
R. F. Rogers ◽  
J. F. Paton ◽  
J. S. Schwaber
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Synaptic Input ◽  
Response Patterns ◽  
Ongoing Activity ◽  
Lung Inflation ◽  
Arterial Blood ◽  
Aortic Nerve ◽  
Mean Pressure ◽  
Central Representation

Central representation of arterial pressure by baroreceptor target neurons in the nucleus of the solitary tract (NTS) has not been studied. The present experiments sought to characterize response patterns of NTS baroreceptive cells in anesthetized, paralyzed, and artificially ventilated rats to both resting pressures and induced blood pressure challenges. Single-unit extracellular recordings were made from 83 baroreceptive NTS cells that received a synaptic input after electrical stimulation of the aortic nerve [latency, 2.46 +/- 0.78 (+/- SD) ms] and were located at an anatomically defined region known to receive baroreceptor afferents. Seventy-one neurons were presumed second order, since they received a short (< 5 ms) and invariant (< +/- 0.5 ms) synaptic input from the ipsilateral aortic nerve. Thirty-five of these neurons were silent at resting blood pressures and produced few (1-4) spikes when presented with induced pressor responses. The remainder (n = 36) had ongoing activity that was not pulse rhythmic and that varied in rate nonuniformly with arterial blood pressure during an induced challenge. Ongoing activity was analyzed for active neurons, revealing both R wave-related and lung inflation-related phasic activity. The present data suggest that baroreceptive NTS neurons may be sensitive to many characteristics of the input signal, such as dP/dt, mean pressure, and cardiac frequency, as well as pulmonary afferent drive.

Arterial pressure control after chronic carotid sinus denervation

1988 ◽  
Vol 255 (4) ◽  
pp. H910-H916 ◽  
Author(s):  
D. S. O'Leary ◽  
A. M. Scher
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Pressure Control ◽  
Base Line ◽  
Baroreflex Control ◽  
Atrial Rate ◽  
Arterial Blood

This study examines the control of arterial blood pressure in conscious, instrumented dogs with atrioventricular block before and greater than or equal to 9 days after carotid sinus baroreceptor denervation. Strength of reflex control of blood pressure was quantitated by measuring the changes in peripheral resistance and atrial rate after square wave changes in cardiac output. Surprisingly, nine or more days after carotid denervation, the strength of baroreflex control of peripheral resistance and atrial rate were not different (P greater than 0.05) from the values before denervation. This was not due to a change in the base-line levels of arterial pressure, atrial rate, cardiac output, or peripheral resistance. Bilateral vagal block after carotid denervation removed reflex effects from remaining baroreceptors and virtually eliminated changes in peripheral resistance in response to changes in arterial pressure. Therefore, the compensatory responses observed after carotid denervation were mediated by the remaining baroreceptors. Thus, after chronic carotid sinus denervation, there is no decrease in the strength of baroreflex control of peripheral resistance or heart rate.

Role of endogenous ANG II and AT1 receptors in regulating arterial baroreflex responses in newborn lambs

1997 ◽  
Vol 272 (6) ◽  
pp. R1862-R1873 ◽  
Author(s):  
J. L. Segar ◽  
A. Minnick ◽  
A. M. Nuyt ◽  
J. E. Robillard
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Ang Ii ◽  
Central Administration ◽  
Arterial Baroreflex ◽  
Response Curves ◽  
Baroreflex Control ◽  
At1 Receptors ◽  
Arterial Blood ◽  
Baroreflex Function

The present study was designed to test the hypothesis that endogenous angiotensin II (ANG II) influences baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) early in life and to determine whether these actions are mediated by angiotensin AT1 or AT2 receptors. To test this hypothesis, we studied the effects of systemic and central administration of losartan, a selective AT1 receptor antagonist, and PD-123319, a selective AT2 antagonist, on baroreflex-mediated control of HR and RSNA in conscious newborn lambs. Systemic administration of losartan decreased resting mean arterial blood pressure (MABP) from 70 +/- 3 to 58 +/- 4 mmHg (P < 0.05) without producing reflex increases in HR or RSNA. The baroreflex response curves were shifted to the left as indicated by a decrease in the arterial pressure at the midpoint of the curve for HR (83 +/- 3 to 75 +/- 4 mmHg) and RSNA (74 +/- 2 to 69 +/- 3 mmHg; P < 0.05 for both). Losartan also reset HR and RSNA baroreflex curves when changes in baseline blood pressure were prevented by simultaneous infusion of phenylephrine. In contrast, a sustained decrease in arterial pressure of 10-12 mmHg with nitroprusside failed to shift the baroreflex function curves. PD-123319 had no effect on baseline HR, MABP, RSNA, or baroreflex responses. Lateral ventricle administration of losartan but not PD-123319 also produced a decrease in arterial pressure (81 +/- 4 to 73 +/- 3 mmHg, P < 0.05) and reset the baroreflex for HR and RSNA toward lower pressure. These results demonstrate that, early in life, endogenous ANG II exerts a tonic effect on baroreflex control of HR and RSNA to shift the curves toward higher pressure levels. The alterations in arterial baroreflex function appear independent of direct ANG II effects on arterial pressure and are mediated by AT1 receptors.

Change in spontaneous baroreflex control of pulse interval during heat stress in humans

2003 ◽  
Vol 95 (5) ◽  
pp. 1789-1798 ◽  
Author(s):  
Kichang Lee ◽  
Dwayne N. Jackson ◽  
Douglas L. Cordero ◽  
Takeshi Nishiyasu ◽  
Jochen K. Peters ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Stroke Volume ◽  
Linear Relationship ◽  
Baroreflex Sensitivity ◽  
Pulse Interval ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Spontaneous Baroreflex

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.

Blood Pressure Variability in Man: Its Relation to High Blood Pressure, Age and Baroreflex Sensitivity

1980 ◽  
Vol 59 (s6) ◽  
pp. 401s-404s ◽  
Author(s):  
G. Mancia ◽  
A. Ferrari ◽  
L. Gregorini ◽  
G. Parati ◽  
G. Pomidossi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Blood Pressure Variability ◽  
Baroreflex Sensitivity ◽  
Variation Coefficient ◽  
Arterial Blood ◽  
Normotensive Subjects

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.

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
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Blood Pressure Variability ◽  
Baroreflex Sensitivity ◽  
Mental Arithmetic ◽  
Pulse Interval ◽  
Hypertensive Subject ◽  
Baroreflex Control

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.

scholarly journals On the Pathology of the dropsy produced by obstruction of the superior and inferior venœ and the portal vein.— Preliminary communication

1907 ◽  
Vol 79 (532) ◽  
pp. 267-283 ◽  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Mean Arterial Blood Pressure ◽  
Normal Limit ◽  
The Body ◽  
Diastolic Filling ◽  
Arterial Blood ◽  
Preliminary Communication ◽  
The Mean

In August, 1903, I published a paper in the ‘Journal of Pathology’(1) in which I demonstrated a method experimentally producing uncompensated hear disease in an animal, which was compatible with life. This method consisted in diminishing the size of the pericardial sac by stitches, so that the diastolic filling of the heart was impeded. The main symptoms of this condition were dropsy and diminution in the amount of urine excreted. As the immediate result of this interference with the action of the heart, there occurred a rise of pressure throughout the whole systemic venous system extending as far back as the capillaries, and a fall of the mean arterial blood-pressure. Further, I found that the pressure in all the veins fell to the normal limit again within the space of about one hour, and that subsequently when dropsy was being produced, the vanous pressure in all parts of the body was normal, and the arterial pressure had almost recovered itself.

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