Central command blunts sensitivity of arterial baroreceptor-heart rate reflex at onset of voluntary static exercise

2006 ◽  
Vol 290 (1) ◽  
pp. H200-H208 ◽  
Author(s):  
Kanji Matsukawa ◽  
Hidehiko Komine ◽  
Tomoko Nakamoto ◽  
Jun Murata
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Central Command ◽  
Arterial Baroreflex ◽  
Static Exercise ◽  
Response Curves ◽  
Stimulus Response ◽  
Aortic Depressor Nerve ◽  
Blood Pressures

We have reported that baroreflex bradycardia by stimulation of the aortic depressor nerve is blunted at the onset of voluntary static exercise in conscious cats. Central command may contribute to the blunted bradycardia, because the most blunted bradycardia occurs immediately before exercise or when a forelimb is extended before force development. However, it remained unknown whether the blunted bradycardia is due to either reduced sensitivity of the baroreflex stimulus-response curve or resetting of the curve toward a higher blood pressure. To determine this, we examined the stimulus-response relationship between systolic (SAP) or mean arterial pressure (MAP) and heart rate (HR) at the onset of and during the later period of static exercise in seven cats ( n = 348 trials) by changing arterial pressure with infusion of nitroprusside and phenylephrine or norepinephrine. The slope of the MAP-HR curve decreased at the onset of exercise to 48% of the preexercise value (2.9 ± 0.4 beats·min−1·mmHg−1); the slope of the SAP-HR curve decreased to 59%. The threshold blood pressures of the stimulus-response curves, at which HR started to fall due to arterial baroreflex, were not affected. In contrast, the slopes of the stimulus-response curves during the later period of exercise returned near the preexercise levels, whereas the threshold blood pressures elevated 6–8 mmHg. The maximal plateau level of HR was not different before and during static exercise, denying an upward shift of the baroreflex stimulus-response curves. Thus central command is likely to attenuate sensitivity of the cardiac component of arterial baroreflex at the onset of voluntary static exercise without shifting the stimulus-response curve.

Reflexes from isolated carotid sinuses of intact and vagotomized conscious dogs

1980 ◽  
Vol 238 (6) ◽  
pp. H815-H822 ◽  
Author(s):  
R. B. Stephenson ◽  
D. E. Donald
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Stimulus Response ◽  
Carotid Baroreflex ◽  
Cervical Vagotomy ◽  
Curve Upward ◽  
Sinus Pressure

Exposure of the vascularly isolated carotid sinuses of 8 conscious dogs to static pressures between 50 and 240 mmHg caused significantly smaller increases [23 +/- 5(SE) mmHg] than decreases (37 +/- 4 mmHg) in arterial pressure frossure and heart rate and shifted the stimulus-response curve upward. Bilateral cervical vagotomy in conscious dogs caused sustained (3 h) increases in arterial pressure (40 +/- 5 mmHg), significantly larger than after atropinization (7 +/- 2 mmHg). In anesthetized, but not in conscious dogs, high sinus pressure reversed the hypertension caused by vagotomy. After vagotomy, low sinus pressure resulted in arterial pressures greater than 200 -mHg. In conscious dogs the carotid baroreflex can widely vary arterial pressure and heart rate despite buffering by extracarotid baroreceptors with vagal afferents, but cannot fully compensate for the acute loss of the latter. Extracarotid baroreceptors actively participate with carotid baroreceptors in the regulation of arterial pressure and better buffer carotid baroreflex-induced increases than decreases in arterial pressure.

scholarly journals Human carotid baroreflex during isometric lower arm contraction and ischemia

1998 ◽  
Vol 275 (3) ◽  
pp. H940-H945 ◽  
Author(s):  
Jonas Spaak ◽  
Patrik Sundblad ◽  
Dag Linnarsson
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Response Curve ◽  
Pressor Response ◽  
Response Curves ◽  
Muscle Ischemia ◽  
Carotid Baroreflex ◽  
Neck Chamber ◽  
Human Carotid

Our aim was to determine the roles of somatomotor activation and muscle ischemia for the tachycardia and hypertension of isometric arm contraction. Carotid-cardiac and carotid-mean arterial pressure (MAP) baroreflex response curves were determined in 10 men during rest, during isometric arm contraction at 30% of maximum, and during postcontraction ischemia. Carotid distending pressure (CDP) was changed by applying pressure and suction in a neck chamber. Pressures ranged from +40 to −80 mmHg and were applied repeatedly for 15 s during the three conditions. Maximum slopes and ranges of the response curves did not differ among conditions. The heart rate (HR) curve was shifted to a 14 ± 1.8 (mean ± SE) beats/min higher HR and a 9 ± 5.7 mmHg higher CDP during contraction and to a 14 ± 5.9 mmHg higher CDP during postcontraction ischemia with no change of HR compared with rest. The MAP curve was shifted to a 20 ± 2.8 mmHg higher MAP and to a 18 ± 5.4 mmHg higher CDP during contraction, and the same shifts were recorded during postcontraction ischemia. We conclude that neither somatomotor activation nor muscle ischemia changes the sensitivity of arterial baroreflexes. The upward shift of the MAP response curve, with no shift of the HR response curve during postexercise ischemia, supports the notion of parallel pathways for MAP and HR regulation in which HR responses are entirely caused by somatomotor activation and the pressor response is mainly caused by muscle ischemia.

Additive Interactions between Propofol and Ketamine When Used for Anesthesia Induction in Female Patients 

1995 ◽  
Vol 82 (3) ◽  
pp. 641-648 ◽  
Author(s):  
T. W. Hui ◽  
T. G. Short ◽  
W. Hong ◽  
T. Suen ◽  
T. Gin ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Additional Term ◽  
Anesthesia Induction ◽  
Response Curves ◽  
Intravenous Anesthesia ◽  
Verbal Command ◽  
Female Patients ◽  
Loss Of Response ◽  
Significant Difference

Background Propofol and ketamine may be paired for anesthesia induction and for total intravenous anesthesia. The nature of any sedative interactions occurring between propofol and ketamine are unknown. The combination when used for anesthesia induction in female patients was studied. Methods Quantal dose-response curves were determined in 180 female patients to whom the drugs were administered individually and in combination. Two minutes after administering the drugs, two endpoints were assessed. First, loss of response to verbal command (hypnosis) and then, in those who failed to respond to this endpoint, loss of response to a 5-s transcutaneous tetanus (anesthesia). Interactions were analyzed by fitting the data to a mathematical model in which response was analyzed in terms of the doses of the two drugs and an additional term included to describe nonadditive interactions. The incidences of apnea, arterial pressure, and heart rate changes during the first 5 min were recorded. Results At the hypnotic endpoint, the ED50s were 1.10 mg/kg propofol (95% CIs 0.93-1.27), 0.39 mg/kg ketamine (95% CIs 0.27-0.46), and the combination of 0.63 mg/kg propofol and 0.21 mg/kg ketamine (95% CIs 0.53/0.18-0.73/0.24). At the anesthetic endpoint, the ED50s were 1.85 mg/kg propofol (95% CIs 1.58-2.36) 0.66 mg/kg ketamine (95% CIs 0.58-0.77), and the combination of 1.05 mg/kg propofol and 0.35 mg/kg ketamine (95% CIs 0.88/0.29-1.27/0.42). The effects were additive at both endpoints; there was no evidence of an interaction. The ED50s for apnea were 1.61 mg/kg propofol (95% CIs 1.39-1.94), greater than 0.85 mg/kg ketamine and for the combination 1.50 mg/kg propofol and 0.50 mg/kg ketamine (95% CIs 1.15/0.38-3.09/1.03). The addition of ketamine did not significantly alter the ED50 for apnea of propofol. There was a significant difference in the arterial pressures among the three groups (P < 0.001). Using the combination, the cardiostimulant effects of ketamine balanced the cardiodepressant effects of propofol. There was no change in arterial pressure or heart rate after the noxious stimulus. Conclusions When using the combination, doses were additive at hypnotic and anesthetic endpoints. Ketamine had no influence on the incidence of apnea after propofol, and the net hemodynamic effects were minimal.

Measurement of sympathetic nerve activity in the unanesthetized rat

1989 ◽  
Vol 67 (1) ◽  
pp. 250-255 ◽  
Author(s):  
J. P. Fluckiger ◽  
G. Gremaud ◽  
B. Waeber ◽  
A. Kulik ◽  
A. Ichino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Blood Pressure Reduction ◽  
Response Curves ◽  
Nerve Activity ◽  
Dose Dependent

A new system was developed in our laboratory to continuously monitor intra-arterial pressure, heart rate, and sympathetic nerve activity in unanesthetized rats. The animals were prepared 24 h before the start of the experiments. Sympathoneural traffic was measured at the level of splanchnic nerve. The amplitude of the spikes recorded at this level was utilized to express sympathetic nerve activity. The amplitude of the residual electroneurogram signal present 30 min after the rats were killed was 32 +/- 2 mV (mean +/- SE; n = 11). For analysis, these background values were subtracted from values determined in vivo. The nerve we studied contains postganglionic fibers, since electrical activity decreased in response to ganglionic blockade with pentolinium (1.25 mg/min iv for 4 min). The amplitude of spikes fell by 43 +/- 4% (n = 4). Sympathetic nerve activity was highly reproducible at a 24-h interval (104 +/- 26 vs. 111 +/- 27 mV for the amplitude of spikes; n = 11). Dose-response curves to the alpha 1-stimulant methoxamine and to bradykinin were established in four rats. The increase in blood pressure induced by methoxamine caused a dose-dependent fall in sympathetic nerve activity, whereas the blood pressure reduction resulting from bradykinin was associated with a dose-dependent activation of sympathetic drive. These data therefore indicate that it is possible with out system to accurately measure sympathetic nerve activity in the awake rat, together with intra-arterial pressure and heart rate.

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.

Arterial baroreflex resetting mediates postexercise reductions in arterial pressure and heart rate

1998 ◽  
Vol 275 (5) ◽  
pp. H1627-H1634 ◽  
Author(s):  
Margaret P. Chandler ◽  
David W. Rodenbaugh ◽  
Stephen E. DiCarlo
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Acute Exercise ◽  
Operating Point ◽  
Arterial Baroreflex ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Single Bout ◽  
Before And After ◽  
The Relationship

We tested the hypothesis that postexercise reductions in arterial pressure and heart rate (HR) are mediated by a lowering of the operating point and a reduction in the gain of the arterial baroreflex. To test this hypothesis, spontaneous changes in arterial pressure and the reflex responses of HR were examined before and after a single bout of mild to moderate dynamic exercise in 19 spontaneously hypertensive rats (SHR, 10 male and 9 female). Eleven SHR subjected to sinoaortic denervation (SAD) (6 male, 5 female) were also studied. All rats were instrumented with an arterial catheter for the measurement of arterial pressure and HR. After exercise, arterial pressure and HR were reduced below preexercise levels. Furthermore, the operating point and spontaneous gain (G) of the arterial baroreflex were reduced. Specifically, after exercise, the spontaneous range of HR (P1, 50%), the pressure at the midpoint of the pressure range (P3, 13%) and the HR at the midpoint of the HR range (H3, 10%), the spontaneous minimum HR (P4, 8%) and maximum HR (10%), and G (76%) were significantly attenuated. SAD significantly attenuated the relationship between arterial pressure and HR by reducing G (males 94%, females 95%). These results demonstrate that acute exercise resulted in a postexercise resetting of the operating point and a reduction in the gain of the arterial baroreflex. Furthermore, these data suggest that postexercise reductions in arterial pressure and HR are mediated by a lowering of the operating point of the arterial baroreflex.

Central command blunts the baroreflex bradycardia to aortic nerve stimulation at the onset of voluntary static exercise in cats

2003 ◽  
Vol 285 (2) ◽  
pp. H516-H526 ◽  
Author(s):  
Hidehiko Komine ◽  
Kanji Matsukawa ◽  
Hirotsugu Tsuchimochi ◽  
Jun Murata
Keyword(s):  
Initial Period ◽  
Body Movement ◽  
Central Command ◽  
Static Exercise ◽  
Sitting Posture ◽  
Depressor Response ◽  
Aortic Depressor Nerve ◽  
Central Inhibition ◽  
Cardiac Component ◽  
The Right

To examine whether the central characteristics of the aortic baroreflex alter from moment to moment during static exercise, we identified the dynamic changes in the sizes of the bradycardia and depressor response evoked by stimulation of the aortic depressor nerve (ADN). Three conscious cats were trained to voluntarily extend the right forelimb and press a bar for 31 ± 1 s with a peak force of 337 ± 22 g while maintaining a sitting posture. The ADN stimulation-induced bradycardia was attenuated at the initial period of exercise (up to 8 s from the exercise onset) to 62 ± 5% of the preexercise bradycardia and remained blunted until the end of exercise. The most blunted bradycardia was observed immediately before or when the forelimb was extended before force development. The baroreflex-induced bradycardia was suppressed again at cessation of exercise when the forelimb was retracted and recovered within a few seconds. In contrast, static exercise did not affect the ADN stimulation-induced depressor response. The ADN stimulation-induced bradycardia was also blunted at the beginning of naturally occurring body movement such as spontaneous postural change or grooming behavior. Thus it is likely that the central characteristics of the aortic baroreflex dynamically change from moment to moment during voluntary static exercise and during natural body movement and that particularly a central inhibition of the cardiac component of the aortic baroreflex is induced by central command at the onset of static exercise, whereas the central property of the vasomotor component of the baroreflex is preserved.

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.

scholarly journals Sex differences in blood pressure responsiveness to spontaneous K-complexes during stage II sleep

2020 ◽  
Author(s):  
Ian Mark Greenlund ◽  
Carl A. Smoot ◽  
Jason R. Carter
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Cardiac Cycle ◽  
Pressor Response ◽  
Systolic Arterial Pressure ◽  
Stage Ii ◽  
Men And Women ◽  
Blood Pressures ◽  
Blood Pressure Responses

K-complexes are a key marker of non-rapid eye movement sleep (NREM), specifically during stages II sleep. Recent evidence suggests the heart rate responses to a K-complexes may differ between men and women. The purpose of this study was to compare beat-to-beat blood pressure responses to K-complexes in men and women. We hypothesized that the pressor response following a spontaneous K-complex would be augmented in men compared to women. Ten men (Age: 23 ± 2 years, BMI: 28 ± 4 kg/m2) and ten women (Age: 23 ± 5 years, BMI: 25 ± 4 kg/m2) were equipped with overnight finger plethysmography and standard 10-lead polysomnography. Hemodynamic responses to a spontaneous K-complex during stable stage II sleep were quantified for 10 consecutive cardiac cycles, and measurements included systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and heart rate. K-complex elicited greater pressor responses in men when blood pressures were expressed as SAP (cardiac cycle × sex: p = 0.007) and DAP (cardiac cycle × sex: p = 0.004). Heart rate trended to be different between men and women (cardiac cycle × sex: p = 0.078). These findings suggest a divergent pressor response between men and women following a spontaneous K-complex during normal stage II sleep. These findings could contribute to sex-specific differences in cardiovascular risk that exist between men and women.

Daily exercise attenuates the sympathetic nerve response to exercise by enhancing cardiac afferents

1997 ◽  
Vol 273 (3) ◽  
pp. H1606-H1610 ◽  
Author(s):  
S. E. DiCarlo ◽  
L. K. Stahl ◽  
V. S. Bishop
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Inhibitory Influence ◽  
Arterial Baroreflex ◽  
Daily Exercise ◽  
Cardiac Afferents ◽  
Response To Exercise ◽  
Renal Sympathetic

"Central command" may initiate the sympathoexcitatory responses at the onset of exercise by shifting the operating point of the arterial baroreflex toward higher pressures. Daily exercise (DE) attenuates the sympathoexcitatory responses to submaximal exercise. This DE-induced adaptation may be due, in part, to an enhanced inhibitory influence of cardiac afferents. This is suggested because cardiac afferents exert a tonic inhibitory influence on the arterial baroreflex which is enhanced by DE. Therefore, the influence of cardiac afferents on the regulation of renal sympathetic nerve activity (RSNA) during exercise was examined in a group of sedentary and age-matched DE rabbits. The rabbits were instrumented with a Silastic catheter inserted into the pericardial sac, electrodes around the renal sympathetic nerves, and catheters in the femoral artery and vein. In the sedentary rabbits, treadmill exercise (12 m/min, 20% grade) significantly increased mean arterial pressure (delta 18 +/- 3 mmHg), heart rate (delta 36 +/- 3 beats/min), and RSNA (delta 295 +/- 23%). More importantly, cardiac afferent blockade (2% intrapericardial procainamide) did not significantly alter the RSNA response to exercise in the sedentary rabbits. DE did not alter the mean arterial pressure (delta 15 +/- 1 mmHg) or heart rate (delta 55 +/- 8 beats/min) response to exercise; however, RSNA (delta 252 +/- 9%) was significantly reduced. In contrast to the sedentary rabbits, cardiac afferent blockade in the DE rabbits significantly increased the RSNA response to exercise (delta 417 +/- 30%). These results suggest that DE attenuates the RSNA response to dynamic exercise due, in part, to an enhanced inhibitory influence of cardiac afferents.

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