scholarly journals Contrasting open-loop dynamic characteristics of sympathetic and vagal systems during baroreflex-mediated heart rate control in rats

2019 ◽  
Vol 317 (6) ◽  
pp. R879-R890 ◽  
Author(s):  
Toru Kawada ◽  
Hiromi Yamamoto ◽  
Yohsuke Hayama ◽  
Takuya Nishikawa ◽  
Kunihiko Tanaka ◽  
...  

Although heart rate (HR) is governed by the sympathetic and parasympathetic nervous systems, a head-to-head comparison of the open-loop dynamic characteristics of the total arc from a baroreceptor pressure input to the HR response has yet to be performed. We estimated the transfer function from carotid sinus pressure input to the HR response ( HCSP→HR) before and after bilateral vagotomy ( n = 7) as well as before and after the administration of a β-blocker propranolol ( n = 8) in anesthetized male Wistar-Kyoto rats. The carotid sinus pressure was perturbed according to a Gaussian white noise signal so that the input power spectra were relatively flat between 0.01 and 1 Hz. The gain plot of HCSP→HR was V-shaped. Vagotomy reduced the dynamic gain at 1 Hz (0.0598 ± 0.0065 to 0.0025 ± 0.0004 beats·min−1·mmHg−1, P < 0.001) but not at 0.01 or 0.1 Hz. β-Blockade reduced the dynamic gain at 0.01 Hz (0.247 ± 0.069 to 0.077 ± 0.017 beats·min−1·mmHg−1, P = 0.020) but not at 0.1 or 1 Hz. We also estimated the efferent limb transfer function from electrical vagal efferent stimulation to the HR response ( HVN→HR) under β-blockade conditions. We associated the model parameters of HVN→HR with the mean HR and the standard deviation of HR so that HVN→HR could be estimated based only on the HR data. We finally estimated the neural arc transfer function from a pressure input to efferent vagal nerve activity by dividing HCSP→HR by HVN→HR. The mathematically determined vagal neural arc showed derivative characteristics with its phase near zero radians at the lowest frequency.

2003 ◽  
Vol 285 (2) ◽  
pp. H833-H840 ◽  
Author(s):  
Koji Kashihara ◽  
Toru Kawada ◽  
Yusuke Yanagiya ◽  
Kazunori Uemura ◽  
Masashi Inagaki ◽  
...  

Although acute myocardial ischemia or infarction may induce the Bezold-Jarisch (BJ) reflex through the activation of serotonin receptors on vagal afferent nerves, the mechanism by which the BJ reflex modulates the dynamic characteristics of arterial pressure (AP) regulation is unknown. The purpose of this study was to examine the effects of the BJ reflex induced by intravenous phenylbiguanide (PBG) on the dynamic characteristics of the arterial baroreflex. In seven anesthetized rabbits, we perturbed intracarotid sinus pressure (CSP) according to a white noise sequence while renal sympathetic nerve activity (RSNA), AP, and heart rate (HR) were recorded. We estimated the transfer function from CSP to RSNA (neural arc) and from RSNA to AP (peripheral arc) before and after 10 min of intravenous administration of PBG (100 μg · kg–1 · min–1). The intravenous PBG decreased mean AP from 84.5 ± 4.0 to 68.2 ± 4.7 mmHg ( P < 0.01), mean RSNA to 76.2 ± 7.0% ( P < 0.05), and mean HR from 301.6 ± 7.7 to 288.4 ± 9.0 beats/min ( P < 0.01). The intravenous PBG significantly decreased neural arc dynamic gain at 0.01 Hz (1.06 ± 0.08 vs. 0.59 ± 0.17, P < 0.05), whereas it did not affect that of the peripheral arc (1.20 ± 0.12 vs. 1.18 ± 0.41). In six different rabbits without intravenous PBG, the neural arc transfer function did not change between two experimental runs with intervening interval of 10 min, excluding the possibility that the cumulative effects of anesthetics had altered the neural arc transfer function. In conclusion, excessive activation of the BJ reflex during acute myocardial ischemia may exert an adverse effect on AP regulation, not only by sympathetic suppression, but also by attenuating baroreflex dynamic gain.


1984 ◽  
Vol 246 (5) ◽  
pp. H696-H701 ◽  
Author(s):  
N. Ishikawa ◽  
C. H. Kallman ◽  
K. Sagawa

To determine the effects of different anesthesias on the performance of the arterial baro-reflex, the open-loop characteristic of the carotid sinus reflex was analyzed in 24 rabbits under anesthesia with pentobarbital (30 mg/kg), urethan (800 mg/kg), alpha-chloralose (80 mg/kg), or a mixture of alpha-chloralose (40 mg/kg) and urethan (0.4 g/kg). For each rabbit and anesthesia, mean systemic arterial pressure and heart rate were measured as carotid sinus pressure was changed in 10-mmHg steps between 40 and 150 mmHg. This set of measurements was repeated four times at 1-h intervals. A logistic function curve was fitted to the carotid sinus pressure-arterial pressure relationship. The parameters of this curve were then analyzed to delineate the specific effects of the anesthesias on the relationship. The main finding was that the response range and the slope parameters under alpha-chloralose anesthesia were significantly smaller than those obtained under the other anesthesias. Propylene glycol, used as the solvent for chloralose, did not affect the reflex control of arterial pressure or heart rate. The reflex under chloralose-urethan anesthesia showed characteristics similar to those under urethan anesthesia. We conclude that although alpha-chloralose has traditionally been used in the dog to obtain strong reflex responses, it weakens the reflex control of arterial pressure in the rabbit.


1998 ◽  
Vol 275 (2) ◽  
pp. H562-H567 ◽  
Author(s):  
Tsutomu Nakahara ◽  
Toru Kawada ◽  
Masaru Sugimachi ◽  
Hiroshi Miyano ◽  
Takayuki Sato ◽  
...  

Recent investigations in our laboratory using a Gaussian white noise perturbation technique have shown that simultaneous sympathetic stimulation augmented the gain of the transfer function from vagal stimulation frequency to heart rate response. However, the mechanism of that augmentation remains to be elucidated. In this study, we examined in anesthetized rabbits how three pharmacological interventions known to cause intracellular accumulation of cAMP affected the transfer function. Isoproterenol (0.3 μg ⋅ kg−1 ⋅ min−1 iv) increased the dynamic gain of transfer function from 7.12 ± 0.67 to 12.4 ± 1.21 beats ⋅ min−1 ⋅ Hz−1( P < 0.05) without changing the corner frequency or the lag time. Similar augmentations were observed when forskolin (5 μg ⋅ kg−1 ⋅ min−1iv) or theophylline (20 mg/kg iv) was administered under conditions of β-adrenergic blockade. These results suggest that the accumulation of cAMP at postjunctional effector sites contributes, at least in part, to the sympathetic augmentation of the dynamic vagal control of heart rate.


2011 ◽  
Vol 300 (1) ◽  
pp. R155-R165 ◽  
Author(s):  
Toru Kawada ◽  
Shuji Shimizu ◽  
Atsunori Kamiya ◽  
Yusuke Sata ◽  
Kazunori Uemura ◽  
...  

Although baroreceptors are known to reset to operate in a higher pressure range in spontaneously hypertensive rats (SHR), the total profile of dynamic arterial pressure (AP) regulation remains to be clarified. We estimated open-loop transfer functions of the carotid sinus baroreflex in SHR and Wistar Kyoto (WKY) rats. Mean input pressures were set at 120 (WKY120 and SHR120) and 160 mmHg (SHR160). The neural arc transfer function from carotid sinus pressure to efferent splanchnic sympathetic nerve activity (SNA) revealed derivative characteristics in both WKY and SHR. The slope of dynamic gain (in decibels per decade) between 0.1 and 1 Hz was not different between WKY120 (10.1 ± 1.0) and SHR120 (10.4 ± 1.1) but was significantly greater in SHR160 (13.2 ± 0.8, P < 0.05 with Bonferroni correction) than in SHR120. The peripheral arc transfer function from SNA to AP showed low-pass characteristics. The slope of dynamic gain (in decibels per decade) did not differ between WKY120 (−34.0 ± 1.2) and SHR120 (−31.4 ± 1.0) or between SHR120 and SHR160 (−32.8 ± 1.3). The total baroreflex showed low-pass characteristics and the dynamic gain at 0.01 Hz did not differ between WKY120 (0.91 ± 0.08) and SHR120 (0.84 ± 0.13) or between SHR120 and SHR160 (0.83 ± 0.11). In both WKY and SHR, the declining slope of dynamic gain was significantly gentler for the total baroreflex than for the peripheral arc, suggesting improved dynamic AP response in the total baroreflex. In conclusion, the dynamic characteristics of AP regulation by the carotid sinus baroreflex were well preserved in SHR despite significantly higher mean AP.


1986 ◽  
Vol 250 (1) ◽  
pp. H96-H107 ◽  
Author(s):  
A. S. Greene ◽  
M. J. Brunner ◽  
A. A. Shoukas

Carotid sinus reflex interactions were studied in 10 dogs anesthetized with pentobarbital sodium. The right and left carotid sinus regions were isolated and perfused at controlled pressures. Pressure in the right and left carotid sinuses were independently varied, and the resulting steady-state reflex changes in arterial pressure, heart rate, respiratory frequency, tidal volume, and total ventilation were measured. Reflex changes when carotid sinus pressure was changed on one side were strongly influenced by pressure in the contralateral carotid sinus (P less than 0.05). Right carotid sinus gain was found to be 0.628 +/- 0.058 at a left carotid sinus pressure of 50 mmHg and 0.148 +/- 0.027 when left carotid sinus pressure was 200 mmHg. Similar results were found for left carotid sinus gain. Suppression was also found for heart rate, respiratory rate, tidal volume, and total ventilation. The hypothesis that rapid resetting of one carotid sinus baroreflex might influence responses from the other side was also tested. Although ipsilateral resetting was consistently observed, no contralateral component of the resetting was detected. An additional inhibitory summation between the right and left carotid sinuses was found such that simultaneous excitation of both receptors resulted in a smaller reflex response than did the sum of individual responses. Sympathetic denervation of the carotid sinus region had no effect.


1980 ◽  
Vol 238 (3) ◽  
pp. H294-H299
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw

The open-loop characteristics of the carotid sinus baroreceptor reflex control of pulsatile arterial pressure-flow relations were studied in halothane-anesthetized dogs. Pressures and flows were measured in the ascending aorta, the celiac, mesenteric, renal, and iliac arteries and were used to compute values of regional vascular impedance and hydraulic power. The carotid sinuses were bilaterally isolated and perfused under conditions of controlled mean pressure with a constant sinusoidal component. Measurements were made with the vagi intact and after bilateral vagotomy. Maximum values of open-loop gain averaged -0.78 +/- 0.08 before and -1.42 +/- 0.20 after vagotomy. Vagotomy produced significant increases in the variation of all hemodynamic variables with carotid sinus pressure that were nonuniformly affected in the various regional vascular beds. Aortic and regional vascular impedance showed significant variations with carotid sinus pressure that were augmented by vagotomy. Aortic impedance exhibited a minimum at the normal set point. These results indicate that a) carotid sinus baroreflexes are well preserved with halothane anesthesia, b) thoracic baroreceptor-mediated reflexes exert significant hemodynamic effects on systemic hemodynamics around normal set point values of arterial pressure, c) systemic baroreceptors exert control over large as well as small vessel properties, and d) the baroreceptor-mediated reflexes produce significant influences on hydraulic power and its components.


1993 ◽  
Vol 264 (4) ◽  
pp. H1215-H1222 ◽  
Author(s):  
L. Hayward ◽  
M. Hay ◽  
R. B. Felder

The effect of prolonged aortic depressor nerve (ADN) stimulation on carotid sinus baroreflex regulation of arterial pressure (AP) and renal sympathetic nerve activity (RSNA) was examined in anesthetized rabbits. Ramp increases in carotid sinus pressure (CSP) were repeated before and after 5 min of bilateral ADN stimulation. One minute after ADN stimulation the curve relating AP to CSP had shifted up and to the right, characterized by significant increases (P < 0.05) in the maximum (91 +/- 2 to 101 +/- 3 mmHg; mean +/- SE), midpoint (118 +/- 7 to 125 +/- 8 mmHg CSP), and minimum (45 +/- 3 to 53 +/- 4 mmHg) of the AP reflex curve. There was a parallel shift downward of the curve relating RSNA to CSP, characterized by significant decreases in the maximum [100 +/- 0 to 66 +/- 8% of maximum control RSNA value (%max)], the range (90 +/- 2 to 59 +/- 8%max), and the gain (-1.0 +/- 0.2 to -0.5 +/- 0.1%max/mmHg) of the RSNA reflex curve. Values returned to control within 10 min of cessation of ADN stimulation. These results suggest that central neurons processing baroreflex information from one set of mechanoreceptors can be reset by convergent signals arising from another baroreceptor site.


1981 ◽  
Vol 240 (3) ◽  
pp. H421-H429 ◽  
Author(s):  
G. Baccelli ◽  
R. Albertini ◽  
A. Del Bo ◽  
G. Mancia ◽  
A. Zanchetti

To evaluate whether sinoaortic afferents contribute to the hemodynamic pattern of fighting, cardiovascular changes associated with fighting were studied in cats before and after sinoaortic denervation. Sinoaortic denervation exaggerates the decrease in heart rate, cardiac output, and arterial pressure during immobile confrontation (hissing, staring but no movement). During nonsupportive fighting (fighting with forelimbs while lying on one side) and supportive fighting ( fighting while standing on four feet) sinoaortic denervation reduces the increase in heart rate and cardiac output, minimizes the mesenteric vasoconstriction, induces a fall in arterial blood pressure, but does not affect iliac vasoconstriction or vasodilatation. The hemodynamic pattern of fighting is similarly changed by temporary inactivation of carotid sinus baroreflexes by common carotid occlusion as by chronic section of sinoaortic nerves. It is concluded that sinoaortic reflexes play an important role in the cardiovascular patterns accompanying natural fighting. They favor cardiac action and allow a marked visceral vasoconstriction to occur, thus minimizing or preventing a fall in blood pressure during emotional behavior.


2002 ◽  
Vol 282 (3) ◽  
pp. H1149-H1156 ◽  
Author(s):  
Toru Kawada ◽  
Can Zheng ◽  
Yusuke Yanagiya ◽  
Kazunori Uemura ◽  
Tadayoshi Miyamoto ◽  
...  

A transfer function from baroreceptor pressure input to sympathetic nerve activity (SNA) shows derivative characteristics in the frequency range below 0.8 Hz in rabbits. These derivative characteristics contribute to a quick and stable arterial pressure (AP) regulation. However, if the derivative characteristics hold up to heart rate frequency, the pulsatile pressure input will yield a markedly augmented SNA signal. Such a signal would saturate the baroreflex signal transduction, thereby disabling the baroreflex regulation of AP. We hypothesized that the transfer gain at heart rate frequency would be much smaller than that predicted from extrapolating the derivative characteristics. In anesthetized rabbits ( n = 6), we estimated the neural arc transfer function in the frequency range up to 10 Hz. The transfer gain was lost at a rate of −20 dB/decade when the input frequency exceeded 0.8 Hz. A numerical simulation indicated that the high-cut characteristics above 0.8 Hz were effective to attenuate the pulsatile signal and preserve the open-loop gain when the baroreflex dynamic range was finite.


1993 ◽  
Vol 74 (4) ◽  
pp. 1748-1754 ◽  
Author(s):  
D. S. O'Leary

Ischemia in active skeletal muscle induces reflex increases in systemic arterial pressure (SAP) and heart rate (HR), termed the muscle metaboreflex. When metaboreflex activation is maintained during postexercise muscle ischemia, SAP remains elevated; however, HR decreases. Why the HR responses differ with metaboreflex activation during exercise vs. during postexercise ischemia while the SAP responses are similar in each setting remains unclear. Two hypotheses were tested: 1) the increase in HR with muscle ischemia occurs predominantly via an increase in sympathetic activity, and 2) sympathetic activity to the heart remains elevated during post-exercise ischemia; however, HR decreases because of an increase in parasympathetic outflow. The muscle metaboreflex was activated in conscious dogs during treadmill exercise (3.2 kph, 0% grade) by progressively decreasing perfusion to the hindlimbs. Experiments were performed before and after muscarinic (atropine) or beta- (atenolol or propranolol) receptor blockade. In control experiments, once beyond the threshold for the reflex, the HR sensitivity of the muscle metaboreflex averaged -2.4 +/- 0.3 beats.min-1.mmHg-1 and the reflex open-loop gain averaged -3.2 +/- 0.3 (calculated as the ratio of the increase in HR or SAP to the decrease in hindlimb perfusion pressure beyond threshold). Atropine had no effect on either HR sensitivity (-2.7 +/- 0.4 beats.min-1.mmHg-1) or open-loop gain (-3.3 +/- 0.5, both P > 0.05 vs. control). However, pretreatment with beta-receptor antagonist significantly decreased both HR sensitivity (-0.7 +/- 0.1 beats.min-1.mmHg-1, P < 0.001) and open-loop gain (-1.9 +/- 0.3, P < 0.01). During postexercise ischemia, HR decreased while SAP remained elevated.(ABSTRACT TRUNCATED AT 250 WORDS)


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