Analysis of heart rate-based control of arterial blood pressure

1996 ◽  
Vol 271 (2) ◽  
pp. H812-H822 ◽  
Author(s):  
W. C. Rose ◽  
J. S. Schwaber
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Vascular System ◽  
Reciprocal Relation ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Limited Effectiveness ◽  
Filling Time

Vagal control of the heart is the most rapidly responding limb of the arterial baroreflex. We created a mathematical model of the left heart and vascular system to evaluate the ability of heart rate to influence blood pressure. The results show that arterial pressure depends nonlinearly on rate and that changes in rate are of limited effectiveness, particularly when rate is increased above the basal level. A 10% change in heart rate from rest causes a change of only 2.4% in arterial pressure due to the reciprocal relation between heart rate and stroke volume; at higher rates, insufficient filling time causes stroke volume to fall. These findings agree well with published experimental data and challenge the idea that changes in heart rate alone can strongly and rapidly affect arterial pressure. Possible implications are that vagally mediated alterations in inotropic and dromotropic state, which are not included in this model, play important roles in the fast reflex control of blood pressure or that the vagal limb of the baroreflex is of rather limited effectiveness.

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.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

The Influence of Physical Activity on Arterial Pressure during Ambulatory Recordings in Man

1980 ◽  
Vol 58 (1) ◽  
pp. 115-117 ◽  
Author(s):  
D. B. Rowlands ◽  
T. J. Stallard ◽  
R. D. S. Watson ◽  
W. A. Littler
Keyword(s):  
Physical Activity ◽  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Ambulatory Blood Pressure ◽  
Physical Activities ◽  
Hypertensive Patients ◽  
Arterial Blood ◽  
Significant Difference ◽  
Hypotensive Therapy

1. Ambulatory blood pressure recordings were made over a 48 h period on six hypertensive patients. The conditions of study were standardized, particularly with regard to physical activity, and during one period of each day the patients were randomly allocated to be active or inactive. 2. Results show that blood pressure was highest during physical activity and lowest during sleep. There was no significant difference between the arterial pressures measured during the same physical activities carried out at the same time each day. However, during the same time on consecutive days when activity was randomized, there was a significant difference between the pressure recordings during physical activity compared with those during inactivity. Heart rate changes showed a similar trend during the randomized period. 3. Physical activity and sleep have a profound effect on continuous arterial blood pressure recordings and these are independent of time alone. These observations should be taken into account when using this ambulatory system to assess hypotensive therapy.

scholarly journals Acute Cardiovascular Effects of Epidural Spinal Cord Stimulation

2007 ◽  
Vol 5;10 (9;5) ◽  
pp. 677-685
Author(s):  
David M. Schultz
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Spinal Cord Stimulation ◽  
Statistical Significance ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Arterial Blood

Background: Several animal studies support the contention that thoracic spinal cord stimulation (SCS) might decrease arterial blood pressure. Objective: To determine if electrical stimulation of the dorsal spinal cord in humans will lower mean arterial pressure (MAP) and heart rate (HR). Design: Case Series Methods: Ten normotensive subjects that were clinically indicated for SCS testing were studied. Two of the 10 patients who underwent testing were excluded from the analysis because they did not respond to the Cold Pressor Test (CPT). Systolic blood pressure, diastolic blood pressure, and heart rate were measured continuously at the wrist (using the Vasotrac device). SCS was administered with quadripolar leads implanted into the epidural space under fluoroscopic guidance. SCS was randomly performed either in the T1-T2 or T5-T6 region of the spinal cord during normal conditions as well as during transient stress induced by CPT. The CPT was conducted by immersing the non-dominant hand in ice-cold water for 2 minutes. Results: There were moderate decreases in MAP and HR during SCS at the T5-T6 region compared to baseline that did not reach statistical significance. However, SCS at the T1-T2 region tended to increase MAP and HR compared to baseline but the change did not reach statistical significance. Arterial blood pressure was transiently elevated by 9.4 ± 3.8 mmHg using CPT during the control period with SCS turned off and also during SCS at either the T1-T2 region or T5-T6 region of the spinal cord (by 9.2 ± 5 mmHg and 10.7 ± 8.4 mmHg, respectively). During SCS at T5-T6, the CPT significantly increased MAP by 5.9±7.1 mmHg compared to control CPT (SCS off). Conclusion: This study demonstrated that SCS at either the T1-T2 or T5-T6 region did not significantly alter MAP or HR compared to baseline (no SCS). However, during transcient stress (elevated sympathetic tone) induced by CPT, there was a significant increase in MAP and moderate decrease in HR during SCS at T5-T6 region, which is not consistent with previous data in the literature. Acute SCS did not result in adverse cardiovascular responses and proved to be safe. Key words: Spinal cord stimulation, mean arterial pressure, heart rate, cold pressor test

Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

2002 ◽  
Vol 282 (1) ◽  
pp. R252-R258 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Whole Body ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Arterial Blood ◽  
The Relationship

To identify whether whole body heating alters arterial baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA and beat-by-beat arterial blood pressure were recorded in seven healthy subjects during acute hypotensive and hypertensive stimuli in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature ( P < 0.01), MSNA ( P < 0.01), heart rate ( P< 0.01), and skin blood flow ( P < 0.001), whereas mean arterial blood pressure did not change significantly ( P > 0.05). During both normothermic and heat stress conditions, MSNA increased and then decreased significantly when blood pressure was lowered and then raised via intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure during heat stress (−128.3 ± 13.9 U · beats−1 · mmHg−1) was similar ( P = 0.31) with normothermia (−140.6 ± 21.1 U · beats−1 · mmHg−1). Moreover, no significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. These data suggest that arterial baroreflex modulation of MSNA and heart rate are not altered by whole body heating, with the exception of an upward shift of these baroreflex curves to accommodate changes in these variables that occur with whole body heating.

Cardioaccelerator action of angiotensin

1962 ◽  
Vol 202 (2) ◽  
pp. 237-240 ◽  
Author(s):  
S. D. Nishith ◽  
L. D. Davis ◽  
W. B. Youmans
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Abdominal Aorta ◽  
Intravenous Infusion ◽  
Control Level ◽  
Arterial Blood ◽  
Initial Decrease ◽  
Slow Intravenous Infusion

Effects of synthetic angiotensin II on heart rate and blood pressure were determined in dogs under the influence of morphine (3 mg/kg) and chloralose (90 mg/kg). Angiotensin in total doses of 2.5–20 µg, rapidly injected intravenously in intact dogs, caused an initial decrease in heart rate followed by a rise above the control level, despite the continued elevation of arterial blood pressure. When the degree of rise in arterial pressure was buffered by a mechanical compensator connected with the abdominal aorta, rapid intravenous angiotensin injection produced no initial cardioinhibitory phase, and the magnitude of the accleration of heart rate was much greater than in the unbuffered animal. Slow intravenous infusion of angiotensin in some cases caused only a rise in heart rate. In sinoaortic denervated animals both blood pressure and heart rate were greatly increased when a total dose of 10 µg angiotensin was rapidly injected intravenously. Thus, it is demonstrated that the cardioinhibitory response to angiotensin depends largely or exclusively on reflex effects from sinoaortic pressoreceptors, and that angiotensin has a strong cardioaccelerator action which is exerted through the efferent nerves to the heart.

scholarly journals Effect of twelve week training program in blood pressure and heart rate at rest in older hypertensive and normotensive women

2017 ◽  
Vol 1 (1) ◽  
pp. 51
Author(s):  
Teuta Osmani Vllasolli
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Training Program ◽  
Older Women ◽  
Experimental Period ◽  
Dynamic Resistance ◽  
Arterial Blood ◽  
Resistance Exercises

Introduction: Epidemiological studies suggest that non-pharmacological       interventions such as exercise may be beneficial for treatment of hypertension.  However the potential benefits of exercises especially resistance training on arterial blood pressure and resting heart rate in older adults without hypertension remain controversial. Objective: To analyze the effect of twelve weeks of training program on systolic blood pressure (SBP) diastolic blood pressure (DBP) mean arterial    pressure (MAP) and heart rate (HR) in older women with and without hypertension. Methods: Seventeen hypertensive women (HW) and 10 normotensive women (NW) were included in training program selected by pre-exercise evaluation of the     cardiovascular status and other risks factors (smoking dislipidemia and diabetes). Training program three times per week was consisted from10 minutes of stretching exercises; 45 minutes of aerobic endurance (gait) and 10 min with five minutes of   relaxation while two times per week were included dynamic resistance exercises  (involving the major muscle groups) The training sessions of resistance exercises were performed in three sets of 8 to 10 repetition of maximum (RM) with rest    interval between sets and exercises of 90 seconds. These days aerobic exercises last only 30minutes.Hemodynamic parameters at rest were evaluated by auscultatory method (mercury sphygmomanometer) and HR by Pulsioxymeter monitor (Polar) before and after twelve weeks of experimental period. Results: The HW group (age 66.8 آ± 5.4 years) and the NW (65.2 آ± 4.8years). In HW was found a reduction of SBP (-10.6mmHgp <0.01) and DBP (-1.94 p=0.043). Although significant reduction were observed in SBP (- 6.7mmHg p<0.05) of NW group there were no significant reduce in DBP after exercises (p=0.0 32). Mean arterial pressure (MAP) and resting HR also didn’t show important changes. Conclusion: Twelve weeks training program consisted of aerobic exercises and dynamic resistance exercises is shown to be an   effective training in reduction of resting SBP in older women with hypertension and also to promote adaptations in the cardiovascular system of normotensive older women without. Keywords: older women blood pressure hypertension normotension heart rate exercise.

Intracoronary epinephrine attenuates baroreflex control of heart rate in the conscious dog

1984 ◽  
Vol 247 (2) ◽  
pp. R237-R245
Author(s):  
M. J. Holmberg ◽  
A. J. Gorman ◽  
K. G. Cornish ◽  
I. H. Zucker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Rate Curve ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Conscious Dog ◽  
Arterial Blood ◽  
The Mean

In the present study, the reflex effects of low-dose (12.5-50 ng X kg-1 X min-1) intracoronary epinephrine infusion on the arterial baroreflex control of heart rate were studied. Mean arterial blood pressure-heart rate curves were constructed by changing mean arterial blood pressure with graded occlusions of the descending aorta and inferior vena cava. Intracoronary epinephrine increased left ventricular dP/dtmax by an average of 309 +/- 67.0 mmHg/s but did not alter resting mean arterial blood pressure or heart rate. Peak sensitivity, the maximum absolute slope along the mean arterial blood pressure-heart rate curve, and heart rate range were 32.7 +/- 3.2 and 26.7 +/- 2.5% less during intracoronary epinephrine compared with control, respectively. Intracoronary epinephrine did not alter the median, threshold, or saturation pressure of the mean arterial blood pressure-heart rate curve. Lidocaine block of the pericoronary nerves, which blocked the ventricular afferent pathway, eliminated the effects of intracoronary epinephrine on the arterial baroreflex. Atropine abolished the effects of intracoronary epinephrine on arterial baroreflex control of heart rate. We conclude that intracoronary epinephrine reflexly attenuates the arterial baroreflex control of heart rate in the conscious dog through activation of ventricular receptors. This response is mediated by cardiac parasympathetic efferents common to both reflex arcs.

Effects of the angiotensin II receptor antagonist Losartan (DuP 753/MK 954) on arterial blood pressure, heart rate, plasma concentrations of angiotensin II and renin and the pressor response to infused angiotensin II in the salt-deplete dog

1992 ◽  
Vol 83 (5) ◽  
pp. 549-556 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Plasma Angiotensin

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1–3 μmin−1 kg−1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min−1kg−1), and a dose of 10 μgmin−1 kg−1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 μmin−1 kg−1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 ± 11.2 to 95.0 ± 12.8 mmHg) and a rise in heart rate (from 84.6 ± 15.1 to 103 ± 15.2 beats/min). Baseline plasma angiotensin II (42.5 ± 11.8 pg/ml) and renin (64.5 ± 92.7 μ-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 ± 11.6 mmHg) was reduced at 15 min (11.8 ± 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 ± 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ngmin−1kg−1, +19.9 ± 8 mmHg; 2000ngmin−1 kg−1, +52.8 ± 13.9 mmHg) with a fall in heart rate (1000 ng min−1 kg−1, −27.9 ± 11.5 beats/min; 2000 ng min−1 kg−1, −31.2 ± 17.3 beats/min). During Losartan infusion the 1000 but not the 2000 ng min−1 kg−1 noradrenaline infusion caused a greater rise in mean arterial blood pressure and a greater fall in heart rate. The fall in heart rate tended to decrease with continued infusion of Losartan. Plasma catecholamine concentrations were unaffected by Losartan. In a further study, higher doses of Losartan (100, 300 and 1000 μg min−1 kg−1; 30 min) produced greater falls in mean arterial blood pressure also with a rise in heart rate and complete blockade of the pressor effect of infused angiotensin II. Some animals became disturbed at the highest dose. 3. Losartan produces rapid dose-related falls in blood pressure and a rise in heart rate and renin release with elevation of plasma angiotensin II. Pressor responses to angiotensin II are reduced at intermediate doses and are eliminated at high doses. Losartan does not appear to inhibit angiotensin II clearance from the plasma and may in some way increase it.

Static muscular contraction elicits a pressor reflex in the chicken

1997 ◽  
Vol 272 (3) ◽  
pp. R759-R765 ◽  
Author(s):  
I. C. Solomon ◽  
T. P. Adamson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Gastrocnemius Muscle ◽  
Muscular Contraction ◽  
Arterial Blood ◽  
Static Contraction ◽  
Stimulation Of

Static muscular contraction has been shown to increase arterial blood pressure and heart rate in humans and other mammals. It is not clear, however, whether birds exhibit a similar response to this maneuver. Therefore, we designed these experiments to determine if the chicken exhibits a cardiovascular response to static muscular contraction and if the observed responses are evoked through a reflex involving muscle afferents. Static contraction of the gastrocnemius muscle was evoked by electrically stimulating the sciatic nerve at 1.5-3.0 times motor threshold (30-40 Hz; 0.025 ms) in 13 chloralose-anesthetized cockerels. We measured arterial blood pressure and muscle tension before and during static contraction and calculated mean arterial pressure and heart rate from the arterial pressure trace. We found that static contraction of the gastrocnemius muscle increased mean arterial pressure from 71 +/- 4 to 95 +/- 4 mmHg (P < 0.05) and increased heart rate from 304 +/- 8 to 345 +/- 10 beats/min (P < 0.05). Furthermore, we found that stimulation of the sciatic nerve after paralysis of the birds with vecuronium bromide or stimulation of the cut peripheral end of the sciatic nerve (using the same stimulation parameters described above) evoked no change in mean arterial pressure or heart rate. We conclude that static muscular contraction of the gastrocnemius muscle in the chicken elicits a pressor response and that this response is due to a reflex arising from the contracting muscles.

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