Comparison of carotid sinus baroreceptors in dogs, cats, monkeys, and rabbits

1984 ◽  
Vol 247 (1) ◽  
pp. R52-R56
Author(s):  
J. P. Gilmore ◽  
E. Tomomatsu
Keyword(s):  
Arterial Pressure ◽  
Single Unit ◽  
Static Pressure ◽  
Carotid Sinus ◽  
Lower Threshold ◽  
Threshold Pressure ◽  
Experimental Conditions ◽  
Single Unit Recordings ◽  
Sinus Pressure

Single-unit recordings were obtained from the vascularly isolated Krebs-Henseleit-perfused carotid sinus of the rabbit and cat, and the results were compared with those obtained previously from the monkey and dog. Carotid sinus pressure was altered using static pressure steps. There was a highly significant correlation between resting arterial pressure and carotid sinus baroreceptor threshold pressure. The baroreceptors of the monkey and rabbit had a significantly lower threshold than those of the dog and cat. The baroreceptors of the monkey had a significantly lower gain than those of the three nonprimates. This is the first study in which baroreceptor activity has been studied under the same experimental conditions in four different species.

Pulsatile activation of baroreceptors causes central facilitation of baroreflex

1989 ◽  
Vol 256 (6) ◽  
pp. H1735-H1741 ◽  
Author(s):  
M. W. Chapleau ◽  
G. Hajduczok ◽  
F. M. Abboud
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Static Pressure ◽  
Carotid Sinus ◽  
Pulse Frequency ◽  
The Other ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Pulsatile Pressure ◽  
Sinus Pressure

The reflex decrease in arterial pressure is greater and more sustained with elevated pulsatile than with elevated static carotid sinus pressure. The purpose of this study was to relate afferent baroreceptor activity (BRA) and efferent sympathetic nerve activity (SNA) during static and pulsatile pressure to evaluate the influence of pulsatile pressure on the central mediation of the baroreflex. The carotid sinuses were isolated in 11 dogs anesthetized with chloralose. Both vagosympathetic trunks were cut and both carotid sinuses exposed to static and pulsatile pressures over a range of mean carotid sinus pressures (40-180 mmHg). BRA was recorded from one carotid sinus nerve, and the other intact carotid sinus served to initiate reflex changes in lumbar or renal SNA and arterial pressure. For the same mean carotid sinus pressure, pulsatile pressure caused significantly greater inhibition of SNA than static pressure. More importantly, for the same or lesser levels of baroreceptor activity per second, pulsatile pressure caused significantly greater inhibition of SNA than static pressure. The inhibition of SNA was not sustained (i.e., there was "adaptation") with continuous baroreceptor input during static pressure, whereas the inhibition of SNA was sustained (i.e., there was no significant adaptation) with the phasic input during pulsatile pressure. Increases in pulse frequency from 1.4 to 2.5 and 3.7 Hz caused progressively less inhibition of SNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute resetting of carotid sinus baroreceptors. II. Possible involvement of electrogenic Na+ pump

1984 ◽  
Vol 247 (5) ◽  
pp. H833-H839 ◽  
Author(s):  
C. M. Heesch ◽  
F. M. Abboud ◽  
M. D. Thames
Keyword(s):  
Single Unit ◽  
Carotid Sinus ◽  
Threshold Pressure ◽  
Carotid Sinus Nerve ◽  
Na Pump ◽  
Electrogenic Na Pump ◽  
Before And After ◽  
K Concentration ◽  
Low K ◽  
Sinus Pressure

In the accompanying manuscript [Am. J. Physiol. 247 (Heart Circ. Physiol. 16): H824-H832, 1984] we demonstrated that a mechanical mechanism alone cannot account for acute resetting of baroreceptors. To determine if changes in the activity of a baroreceptor electrogenic Na+ pump contributed to resetting, single-unit baroreceptor discharge was recorded from the carotid sinus nerve while resetting protocols were performed before and after exposing the vascularly isolated carotid sinus to treatments known to block the Na+ pump [ouabain and low extracellular K+ concentration ([K+]o)]. Ouabain (0.1-0.5 microgram/ml) blocked the increase in baroreceptor threshold pressure that occurred when intrasinus pressure was increased by 30 mmHg for 15 min [delta threshold = 16 +/- 3 (SE) mmHg before and 1.2 +/- 2.3 mmHg after ouabain]. In 12 experiments carotid sinus pressure was increased from 70 to 160 mmHg for 5 min and then returned to 70 mmHg for 10 min in the presence of both normal [K+]o (5.8 mM) and low [K+]o. Exposure to the low K+ solution resulted in a significantly smaller increase in threshold pressure when intrasinus pressure was increased from 70 to 160 mmHg (9 +/- 2.7 vs. 18 +/- 2.1 mmHg). When K+ was replaced, threshold pressure again increased by 18 +/- 2.3 mmHg, the increase in threshold was reversed. Thus, since ouabain blocked and low [K+]o attenuated acute resetting of the baroreceptors, we propose that changes in the activity of an electrogenic Na+ pump contribute to acute resetting.

Carotid sinus control of pulsatile hemodynamics in halothane-anesthetized dogs

1980 ◽  
Vol 238 (3) ◽  
pp. H294-H299
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Open Loop ◽  
Hydraulic Power ◽  
Set Point ◽  
Hemodynamic Variables ◽  
Vascular Impedance ◽  
Mean Pressure ◽  
Anesthetized Dogs ◽  
Sinus Pressure

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.

Suppression of baroreceptor discharge by endothelin at high carotid sinus pressure

1992 ◽  
Vol 263 (1) ◽  
pp. R103-R108 ◽  
Author(s):  
M. W. Chapleau ◽  
G. Hajduczok ◽  
F. M. Abboud
Keyword(s):  
Endothelial Cells ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
High Dose ◽  
Nerve Activity ◽  
Local Exposure ◽  
Potent Vasoconstrictor ◽  
Alpha Chloralose ◽  
Vasoconstrictor Peptide ◽  
Sinus Pressure

Endothelin is a potent vasoconstrictor peptide released from endothelial cells capable of producing marked and prolonged increases in arterial pressure. The purpose of this study was to determine whether endothelin alters the sensitivity of arterial baroreceptors. Multifiber baroreceptor activity was recorded from the vascularly isolated, endothelium-denuded carotid sinus in dogs anesthetized with alpha-chloralose. Local exposure of baroreceptors to endothelin at a concentration of 10(-8) M produced vasoconstriction of the carotid sinus as measured with sonomicrometer crystals but did not alter baroreceptor discharge significantly. A higher concentration of endothelin (10(-7) M) markedly suppressed baroreceptor activity, particularly at pressures greater than 100 mmHg (n = 7, P less than 0.05). The magnitude of the decrease in activity was dependent on the duration of exposure to endothelin. Baroreceptor activity measured at carotid pressures of 60, 100, and 200 mmHg averaged 23 +/- 4, 65 +/- 6, and 100 +/- 0% of maximum during control; 38 +/- 12, 61 +/- 9, and 74 +/- 15% after exposure to endothelin (10(-7) M) for 2 min; and 27 +/- 8, 53 +/- 12, and 56 +/- 19% after 12 min, respectively. The suppression of nerve activity with the high dose of endothelin was not accompanied by additional vasoconstriction, suggesting a direct effect of endothelin on nerve endings. We speculate that endothelin released from endothelial cells may act in a paracrine manner to suppress activity of baroreceptors, particularly at high levels of arterial pressure. Such an action would interfere with the buffering capacity of the baroreflex and promote hypertension.

Aortic arch reflex control of total systemic vascular capacity

1987 ◽  
Vol 253 (3) ◽  
pp. H598-H603
Author(s):  
A. A. Shoukas ◽  
M. J. Brunner ◽  
A. S. Greene ◽  
C. L. MacAnespie
Keyword(s):  
Arterial Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Reservoir Volume ◽  
Aortic Arch Pressure ◽  
Pressure Changes ◽  
Change In Mean ◽  
Sinus Pressure

The ability of the aortic arch baroreceptors to change vascular capacity was measured and, in the same animal, compared with carotid sinus reflex changes in capacity. Seven dogs were anesthetized with pentobarbital sodium and perfused with constant flow. Changes in external reservoir volume reflected reciprocal changes in total systemic vascular capacity and changes in arterial pressure parallel changes in total peripheral resistance. The aortic arch and carotid sinus baroreceptor areas were isolated, and the pressures were controlled separately. With carotid sinus pressure held constant at 125 mmHg, aortic arch pressure was increased and decreased between 225 and 50 mmHg, and the changes in reservoir volume and systemic arterial pressure were measured. Results from increasing and decreasing aortic arch or carotid sinus pressure were not significantly different and were averaged. The mean change in reservoir volume was 1.9 +/- 0.2 ml/kg and the change in mean arterial pressure was 18.7 +/- 3.7 mmHg. The changes in reservoir volume and arterial pressure caused by the aortic arch reflex were not influenced by the level of carotid sinus pressure. Carotid sinus pressure changes between 200 and 50 mmHg at a constant aortic arch pressure caused reservoir volume and arterial pressure to change by 7.2 +/- 0.9 ml/kg and 45.1 +/- 4.1 mmHg, respectively. The level of aortic arch pressure did not modify these responses.

Pulsatile sinus pressure changes evoke sustained baroreflex responses in awake dogs

1988 ◽  
Vol 255 (3) ◽  
pp. H673-H678 ◽  
Author(s):  
D. Mendelowitz ◽  
A. M. Scher
Keyword(s):  
Arterial Pressure ◽  
Pulse Pressure ◽  
Carotid Sinus ◽  
Pressure Change ◽  
Conscious Dogs ◽  
Reflex Responses ◽  
Depressor Response ◽  
Pulsatile Pressure ◽  
Pressure Changes ◽  
Sinus Pressure

A modified Stephenson-Donald preparation was used to control pressure in an isolated carotid sinus in conscious dogs with all other arterial baroreceptors denervated. Sinus pressure was changed from preisolation control levels to either an elevated static or an elevated pulsatile pressure for 5 min. These sinus pressure changes evoked similar initial decreases in arterial pressure. The elevated static sinus pressure (150 or 175 mmHg) caused an initial depressor response of -32.7 +/- 5.5 mmHg, which then decayed rapidly. Five minutes after the change in sinus pressure, the depressor response was abolished, as arterial pressure returned to control pressure. This decay of the response would be expected if resetting occurred. In contrast, when the sinus was exposed to elevated pulsatile pressures (125 or 150 mmHg mean, 50 mmHg pulse pressure) depressor responses were sustained throughout the sinus pressure change (-23.2 +/- 5.3 mmHg initial, -29.0 +/- 4.8 mmHg at 5 min; P greater than 0.4). These results demonstrate that while the reflex responses rapidly reset to elevated static sinus pressures, elevated pulsatile pressures elicit sustained reflex responses.

Effect of cervical sympathetic nerve stimulation on canine carotid sinus reflex

1976 ◽  
Vol 230 (4) ◽  
pp. 1026-1030 ◽  
Author(s):  
CP Bolter ◽  
Ledsome
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Carotid Sinus ◽  
Full Range ◽  
Systemic Arterial Pressure ◽  
Reflex Response ◽  
Cervical Sympathetic ◽  
Pressure Changes ◽  
Cervical Sympathetic Nerve ◽  
Sinus Pressure

In the chloralose-anesthetized dog the carotid sinus on one side of the neck was isolated vascularly. Pressure in the isolated sinus [carotid sinus pressure (CSP)], electrocardiogram, and systemic arterial pressure were recorded. Both vagosympathetic trunks were cut and the contralateral common carotid artery was occluded or the contralateral sinus nerve was cut to reduce reflex buffering of arterial pressure changes. By varying CSP from 50 to 250 mmHg the full range of the reflex response was examined. Electrical stimulation of the peripheral end of the cut ipsilateral cervical sympathetic nerve brought about a rapid decrease in mean arterial pressure (MAP) and heart rate (HR) at lower CSPs, no change in these variables at midrange CSPs, and a gradual increase at higher CSPs, such that the gain of the reflex was reduced (1.89 +/- 0.19 to 1.33 +/- 0.15 mmHg/mmHg). The decrease in MAP and HR at lower CSPs implies an increase in baroreceptor activity whereas the converse would appear to occur at higher CSPs. These responses attained a maximum value at low stimulus frequencies (less than 10 Hz).

Baroreflex unimpaired by operant avoidance or classical aversive conditioning in dogs

1988 ◽  
Vol 254 (6) ◽  
pp. R1025-R1034
Author(s):  
R. A. Shammas ◽  
A. L. Denison ◽  
T. W. Pfennig ◽  
D. P. Hemker ◽  
R. B. Stephenson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Classical Conditioning ◽  
Operant Conditioning ◽  
Avoidance Conditioning ◽  
Carotid Sinus ◽  
Aversive Conditioning ◽  
Shock Avoidance ◽  
Classical Aversive Conditioning ◽  
Sinus Pressure

Previous studies showed that baroreflex control of heart rate is impaired during operant shock avoidance conditioning and classical aversive conditioning. However, the effects of such "emotionally stressful" paradigms on the ability of the baroreflex to control arterial pressure have not been directly assessed. We prepared the carotid sinus regions of dogs for reversible isolation from the systemic circulation, and we derived complete stimulus-response relations for the effects of carotid sinus pressure on both heart rate and arterial pressure. For any given carotid sinus pressure, arterial pressure and heart rate were higher during operant shock-avoidance conditioning and during classical aversive conditioning than in a neutral environment, which indicates an upward resetting of the baroreflex. However, threshold and saturation carotid sinus pressures were unaffected by operant conditioning or classical conditioning, which indicates that the baroreceptors themselves were not reset. The ranges over which the carotid baroreflex could vary arterial pressure and heart rate were significantly increased during both operant conditioning and classical conditioning. Baroreflex gain was unchanged during operant conditioning and was significantly increased during classical conditioning. We conclude that the baroreflex is not impaired during operant shock-avoidance conditioning or classical aversive conditioning in dogs. However, the baroreflex is reset and regulates blood pressure at an elevated level.

Rabbit carotid sinus reflex under pentobarbital, urethan, and chloralose anesthesia

1984 ◽  
Vol 246 (5) ◽  
pp. H696-H701 ◽  
Author(s):  
N. Ishikawa ◽  
C. H. Kallman ◽  
K. Sagawa
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Logistic Function ◽  
Systemic Arterial Pressure ◽  
Open Loop ◽  
Specific Effects ◽  
Reflex Control ◽  
Alpha Chloralose ◽  
Sinus Pressure

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.

Simultaneous encoding of carotid sinus pressure and dP/dt by NTS target neurons of myelinated baroreceptors

1996 ◽  
Vol 76 (4) ◽  
pp. 2644-2660 ◽  
Author(s):  
R. F. Rogers ◽  
W. C. Rose ◽  
J. S. Schwaber
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Nucleus Tractus Solitarius ◽  
Firing Frequency ◽  
Second Order ◽  
Rate Of Change ◽  
Surrounding Tissue ◽  
Absolute Pressure ◽  
Mean Pressure ◽  
Sinus Pressure

1. We seek to understand the baroreceptor signal processing that occurs centrally, beginning with the transformation of the signal at the first stage of processing. Because quantitative descriptions of the encoding of mean arterial pressure and its derivative with respect to time by baroreceptive second-order neurons have been unavailable, we characterized the responses of nucleus tractus solitarius (NTS) neurons that receive direct myelinated baroreceptor inputs to combinations of these two stimulus variables. 2. In anesthetized, paralyzed, artificially ventilated rabbits, the carotid sinus was vascularly isolated and the carotid sinus nerve was dissected free from surrounding tissue. Single-unit extracellular recordings were made from NTS neurons that received direct (with the use of physiological criteria) synaptic inputs from carotid sinus baroreceptors with myelinated axons. The vast majority of these neurons did not receive ipsilateral aortic nerve convergent inputs. With the use of a computer-controlled linear motor, a piecewise linear pressure waveform containing 32 combinations of pressure and its rate of change with respect to time (dP/dt) was delivered to the ipsilateral carotid sinus. 3. The average NTS firing frequency during the different stimulus combinations of pressure and dP/dt was a nonlinear and interdependent function of both variables. Most notable was the "extinctive" encoding of carotid sinus pressure by these neurons. This was characterized by an increase in firing frequency going from low to medium mean pressures (analyzed at certain positive dP/dt values) followed by a decrease in activity during high-pressure stimuli. All second-order neurons analyzed had their maximal firing rates when dP/dt was positive. 4. All neurons had their maximal firing frequency locations ("receptive field centers") at just 3 of 32 possible pressure-dP/dt coordinates. The responses of a small population of neurons were used to generate a composite description of the encoding of pressure and dP/dt. When combined as a composite of individually normalized values, the encoding of carotid sinus pressure and dP/dt may be approximated with the use of two-dimensional Gaussian functions. 5. We conclude that the population of NTS neurons recorded most faithfully encodes the rate and direction of (mean) pressure change, as opposed to providing the CNS with an unambiguous encoding of absolute pressure. Instead, the activity of these neurons, individually or as a population, serves as an estimate for the first derivative of the myelinated baroreceptor signal's encoding of mean pressure. We therefore speculate that the output of these individual neurons is useful in dynamic, rather than static, arterial pressure control.

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