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Vol. 84, Issue 4, 1158-1165, April 1998
Departments of 1 Physiology and 2 Internal Medicine, Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, Texas 75235-9034; and 3 Department of Exercise Science, University of South Carolina, Columbia, South Carolina 29208
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ABSTRACT |
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Top
Abstract
Introduction
Methodology
Results
Discussion
References
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To determine the potential of an inhibitory interaction between the carotid sinus baroreflex (CSB) and the exercise pressor reflex (EPR), both pathways were activated to produce sympathoexcitation. It was hypothesized that, under conditions when the baroreflex increased sympathetic outflow, the interaction between CSB and EPR would be inhibitory. Bilateral carotid occlusion (BCO), electrically induced muscle contraction (EMC), and passive muscle stretch (PMS) were used to evoke sympathoexcitation. BCO decreased sinus pressure 50 ± 5 mmHg, and the levels of muscle tension generated by EMC and PMS were 7 ± 2 and 8 ± 1 kg, respectively. This resulted in significant increases in mean arterial pressure (MAP) of 55 ± 9, 50 ± 7, and 50 ± 6 mmHg (P = not significant, BCO vs. EMC vs. PMS) and in heart rate (HR) of 7 ± 2, 19 ± 4, and 17 ± 2 beats/min (P < 0.05, BCO vs. EMC and PMS). When BCO was combined with EMC or PMS, the reflex increase in MAP was augmented (80 ± 8 and 79 ± 10 mmHg; BCO+EMC and BCO+PMS, respectively; P < 0.05). However, summation of the individual MAP responses was greater than the response evoked during coactivation (106 ± 11 and 103 ± 12 mmHg, respectively, P < 0.05). Because summing the individual blood pressure responses exceeded the response during coactivation, the net effect was that the CSB and EPR interacted in an occlusive manner. In contrast, summation of the individual chronotropic responses was the same as the response evoked during coactivation. Moreover, there was no difference in summation of the individual MAP or HR responses when muscle afferents were activated by either EMC or PMS. In conclusion, the interaction between the CSB and the EPR in control of MAP was occlusive when both reflexes were stimulated to evoke sympathoexcitation. However, summation of the reflex changes in HR was simply additive.
static muscle contraction; baroreceptor afferents; somatic afferents; sympathetic nerve activity; heart rate; blood pressure; exercise
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INTRODUCTION |
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Top
Abstract
Introduction
Methodology
Results
Discussion
References
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NEURAL INPUT from three principal sources establishes the autonomic and cardiovascular adjustments to exercise (19, 27, 34). These sources include 1) descending input from supramedullary regions (central command), 2) ascending input from contracting skeletal muscle (exercise pressor reflex), and 3) afferent input from peripheral baroreceptor populations (arterial and cardiopulmonary baroreceptors). The cardiovascular responses mediated by each of these neural pathways have been well described (3, 17, 19, 22, 25, 27, 34, 36, 38). However, the effect of simultaneously activating two or more of these pathways is complex, and the central integration of these neural inputs is not well understood.
Previous studies have reported that tetanic (35) and rhythmic muscle contraction (31, 36) potentiated the reflex sympathoexcitation when afferent input from arterial baroreceptors was prevented by acute baroreceptor deafferentiation. From this finding, it has been suggested that arterial baroreceptor afferent input acts as an inhibitory signal during exercise to oppose sympathoexcitation (26, 31, 32, 35, 36). However, others have shown that systemic pressure falls in the absence of afferent input from arterial baroreceptors (2, 7, 13, 16). This has been taken as evidence that neural input from arterial baroreceptors acts as an excitatory signal and, together with the exercise pressor reflex and central command, increases sympathetic outflow during exercise. Neural input from arterial baroreceptors and skeletal muscle receptors is conveyed to the central nervous system (CNS) via separate afferent pathways. However, the central projections of these two cardiovascular reflexes synapse in similar regions of the medulla (9, 10, 14, 33), and they share common efferent sympathetic pathways and effector organs (3, 17, 19, 28). Therefore, summation of the sympathoexcitatory responses evoked by these two reflexes will depend on the degree of overlap between these central and efferent neural pathways. The motivation for this study was to determine whether the interaction between the arterial baroreflex and the exercise pressor reflex was inhibitory when both pathways evoked sympathoexcitation. In this context, the baroreflex and the exercise pressor reflex represent two redundant sympathoexcitatory reflex pathways, and the inhibitory interaction between them may occur at a central or a peripheral site. To evoke a sympathoexcitatory response, the carotid baroreflex was selectively inhibited by decreasing the perfusion pressure to the carotid sinus regions (bilateral carotid occlusion), and the exercise pressor reflex was activated by passive stretch and electrically induced contraction of the triceps surae. We tested the hypothesis that, under the condition when both reflex pathways increased sympathetic outflow, the interaction between the baroreflex and the exercise pressor reflex would be inhibitory. To determine whether the interaction occurred at a peripheral (i.e., level of the effector organs) or at a central (i.e., common central/efferent pathway) site, the reflex cardiovascular responses were compared with the responses evoked by CNS ischemia. It was reasoned that if the interaction was of central origin, the reflex cardiovascular responses evoked by both reflexes would be less than the response evoked during CNS ischemia [a maneuver known to elicit maximal changes in blood pressure and heart rate (HR)]. Furthermore, this would eliminate the possibility that the inhibitory interaction between these two reflexes was caused simply by saturation of the common effector organs (i.e., heart, resistance vessels) that produced the increase in blood pressure and HR. A preliminary report of these findings has been published (24).
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METHODOLOGY |
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Top
Abstract
Introduction
Methodology
Results
Discussion
References
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Surgical procedures.
The experiments were conducted on 11 mongrel cats of either sex (body
wt 3.0-5.5 kg). After initial induction of anesthesia with a gas
mixture [3-5% halothane in oxygen (1-2 l/min)],
a solution of 
-chloralose (80 mg/kg) and urethan (200 mg/kg) was
administered intravenously via a femoral vein. Catheters
(polyethylene tubing, PE-60) were inserted into the left femoral vein
for the administration of drugs and the left femoral artery for
measurement of systemic arterial pressure. Animals were artificially
ventilated by a mechanical respirator (model 661, Harvard Apparatus,
South Natick, MA). Arterial blood gases and pH were measured every
45-60 min by an automated blood-gas analyzer (model ABL-3,
Radiometer) and maintained within normal ranges (arterial
PO2 80-100 Torr, arterial
PCO2 35-45 Torr, pH
7.3-7.4). If necessary, 100% oxygen was supplemented to maintain arterial PO2 above 80 Torr. Rectal temperature was continuously monitored throughout each
experiment and was maintained between 37 and 38°C by a
temperature-controlled water-perfused heating pad and a
near-infrared-heat lamp. Gradual increases in baseline HR and blood
pressure over the course of the experiment were used to indicate the
need for additional anesthesia. When supplemental anesthesia was
required, a solution of -chloralose (15 mg/kg) and urethan (75 mg/kg) was administered intravenously. Next, a laminectomy was
performed, exposing the lower lumbar and upper sacral portions of the
spinal cord from roughly L5 to
S2.
Data acquisition. Systemic arterial pressure and CSP were measured by connecting the femoral artery and external carotid artery catheters to separate pressure transducers (model P23ID, Statham, Oxnard, CA). MAP was calculated from an algorithm run on a laboratory minicomputer (model PDP-11/23, Digital Equipment, Maynard, MA), which integrated the area under the arterial pressure waveform. HR was derived by a biotachometer (Gould Instruments, Cleveland, OH) from the systemic arterial pulse pressure as well as from the sequential timing of R-R intervals from surface electrocardiogram. All data were simultaneously recorded on an eight-channel physiological recorder (model 2800S, Gould Instruments) as well as a videotape multiplex adaptor (model 4000, Vetter, Rebersburg, PA) and recorder (model PV-4760, Panasonic) system. The cardiovascular signals were acquired by a laboratory minicomputer (model PDP-11/23, Digital Equipment) at a sampling frequency of 100 Hz by an asynchronous data-acquisition program for subsequent analysis. Off-line analyses were performed by sorting the data into 6-s bins and averaging the beat-to-beat changes in HR and MAP over the course of each experimental trial.
Experimental protocol. On completion of the surgery and positioning the animal in the head and spinal units, a period of 60 min was used to permit MAP and HR to stabilize. Reflex changes in HR and MAP were measured during 1) activation of muscle mechano- and metaboreceptors by static muscle contraction and/or passive muscle stretch and 2) inhibition of the carotid sinus baroreflex by occlusion of the common carotid arteries. First, electrically induced static muscle contraction of the triceps surae was performed by stimulating the L7 and S1 ventral roots for 1 min at a frequency of 30-40 Hz, a pulse duration of 0.1 ms, and a voltage representing 2.5-3.0 times the motor threshold with the muscle preloaded with 0.8-1.0 kg of tension. Use of these stimulation parameters, in conjunction with determination of the motor threshold before each tetanic muscle contraction, has been shown to elicit consistent muscular force generation during electrically induced tetanic contraction that is mediated exclusively by group III and group IV muscle afferents (17). Passive stretch of the triceps surae was performed to the same level of muscle tension generated during ventral root stimulation. A period of no less than 15 min separated each condition to permit HR and MAP to return to their prestimulus baseline values. Second, the carotid baroreceptor reflex was activated for 1 min by simultaneously inflating the vascular occluders on the common carotid arteries, which rapidly reduced CSP below the threshold of the baroreflex (28). Third, the carotid baroreflex and the exercise pressor reflex were simultaneously activated for 1 min as previously outlined. Fourth, static muscle contraction, passive muscle stretch, and bilateral carotid occlusion (BCO) were again performed to determine the extent of deterioration of the preparation over the duration of the experiment. In the event that the reflex change in blood pressure during muscle contraction/stretch was <80% of the initial response, it was deemed that the preparation had deteriorated, and no further trials were performed. If, however, the cardiovascular responses had not deteriorated, the above-mentioned sequence was repeated. On average, this sequence was repeated twice, and the reflex cardiovascular responses were averaged to provide a mean response for each animal. The order of presentation of these four experimental treatments was randomized. Because the order did not appear to have an effect on the reflex-evoked cardiovascular responses, these data were combined. Finally, an intravenous injection (200 µg/kg) of the neuromuscular-blocker pancuronium bromide (Elkins-Sinn, Cherry Hill, NJ) was administered to confirm that the induced cardiovascular response was a reflex originating in the hindlimb skeletal muscle. The paralyzing agent was given 5 min before electrically induced muscle contraction.
Temporary occlusion of the vertebral and common carotid arteries was performed for 15-20 s to evoke CNS ischemia. This maneuver was performed to evoke maximal sympathoexcitation to determine whether the response of the effector organs (i.e., heart, vascular smooth muscle) was saturated during high levels of sympathoexcitation. This procedure was repeated twice, and the changes in MAP and HR were averaged to obtain a mean response for each animalStatistical analyses. The reflex changes in MAP, CSP, HR, and developed muscle tension during electrically induced muscle contraction/passive muscle stretch and baroreflex activation were averaged in 10-s time bins during a period of 40 s preceding reflex activation, continuously over the 60 s of activation, and over the 20 s immediately after reflex activation. Changes in these variables from control levels were compared by a two-way analysis of variance (ANOVA) with repeated-measures [experimental condition (3 levels) × time (12 levels)]. When a significant main effect was found, differences were identified by using a Student-Newman-Kuels multiple-comparison test.
To identify the nature of the interaction between the carotid baroreflex, and the skeletal muscle reflex the peak changes in HR and MAP elicited during coactivation were compared by summing the individual peak cardiovascular responses evoked when each reflex was activated separately. The peak cardiovascular responses evoked by baroreceptor afferents, skeletal muscle afferents, and algebraic summation and during CNS ischemia were compared by a one-way ANOVA. Data are presented as means ± SE. The level of significance was set at P < 0.05.| |
RESULTS |
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Top
Abstract
Introduction
Methodology
Results
Discussion
References
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Reflex changes in MAP and HR by carotid sinus baroreceptors and skeletal muscle mechano- and metaboreceptors. Baseline values and peak changes in MAP and HR to baroreceptor activation and muscle contraction are summarized in Table 1. No significant difference was found in baseline HR and MAP between the experimental conditions (i.e., BCO, muscle contraction, reflex coactivation) or in the level of developed muscle tension during contraction alone and coactivation [P = not significant (NS)]. The time course and characteristic profile of reflex responses evoked by activation of skeletal muscle receptors and carotid baroreceptors by electrically induced tetanic muscle contraction and BCO are depicted in Fig. 1. There was a gradual increase in MAP and HR, and the maximal change in each variable was reached ~30-40 s after onset of the stimulus (time = 0 s). The peak changes in MAP and HR to muscle contraction and BCO are presented in Table 1 and illustrated in Fig. 2. The peak increase in MAP and HR (10-s epochs) to muscle contraction was 50.2 ± 7.0 mmHg and 18.6 ± 3.5 beats/min, respectively (P < 0.05). The reflex increase in MAP evoked by BCO was similar to the response to muscle contraction (54.7 ± 8.5 mmHg; P < 0.05). However, the reflex tachycardia to BCO was significantly less than that produced by muscle contraction (8.1 ± 2.3 beats/min; P < 0.05). Coactivation of carotid baroreflex and the exercise pressor reflex augmented the reflex changes in MAP and HR. The peak rise in MAP and HR (79.5 ± 7.6 mmHg and 26.0 ± 4.0 beats/min, respectively) was significantly greater than the changes evoked when each reflex was activated separately (P < 0.05).
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Effect of CNS ischemia and muscle paralysis on reflex cardiovascular responses. We evoked CNS ischemia to induce a maximal level of sympathoexcitation and contrasted the changes in MAP and HR with those produced during activation of the baroreflex and the exercise pressor reflex. CNS ischemia increased MAP and HR (133.3 ± 5.6 mmHg and 35.2 ± 4.0 beats/min, respectively; P < 0.05). These responses were significantly larger than both the evoked responses during simultaneous activation of both reflexes and the algebraic summation of the individual responses (see Figs. 2 and 4).
To determine whether the cardiovascular response elicited by electrical stimulation of L7 and S1 ventral roots was mediated by activation of sensory receptors originating in the contracting skeletal muscle, the effect of muscle paralysis with pancuronium bromide (200 µg/kg) was examined. After intravenous injection of the neuromuscular-blocking agent, the reflex increase in MAP and HR to electrical stimulation of L7 and S1 ventral roots was abolished. However, the reflex responses to BCO were preserved during paralysis.| |
DISCUSSION |
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Top
Abstract
Introduction
Methodology
Results
Discussion
References
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The interaction between arterial baroreceptors and skeletal muscle has previously been examined (1, 26, 31, 32, 35, 36). However, the anatomic substrate(s) mediating this interaction remains unknown. The present study found an inhibitory interaction in the regulation of arterial blood pressure when the baroreflex and the exercise pressor reflex were activated to evoke excitatory sympathetic responses. Because the cardiovascular response to CNS ischemia exceeded the response evoked by simultaneous activation of both reflexes, saturation of effector organs (i.e., chronotropic/inotropic responses and vascular smooth muscle vasoconstriction) was excluded as the primary site for inhibition between these two pathways. Therefore, the major new finding of this study is that the likely site for inhibition between these two reflexes is within the CNS.
Inhibitory summation for blood pressure control. The present study found that the sympathetically mediated responses summated in an inhibitory manner. This supports the findings from earlier studies (31, 35). However, Walgenbach and Donald (36) reported that when carotid baroreceptors were surgically isolated and perfused at a constant pressure the exercise-induced increase in blood pressure was potentiated when the dogs ran on a treadmill. They attributed this potentiated response to a marked vasoconstriction within the nonexercising vascular beds mediated by an increase in sympathetic neural activity. Thus, when carotid baroreceptors remain intact and are unable to respond to changes in blood pressure, the increase in blood pressure evoked during exercise was augmented. This exaggerated sympathetic neural response was supported by our finding that the increase in MAP and HR was greater when the exercise pressor reflex and the carotid sinus baroreflex were activated to mutually evoke sympathoexcitation.
However, the combined effect of inhibiting the carotid sinus baroreflex and activating the skeletal muscle receptors yielded responses that were significantly less than when each afferent pathway was activated separately. The summation of inputs from multiple neural pathways depends on whether the sensory inputs are excitatory or inhibitory (1, 28). Sagawa (28) found that the interaction between selected baroreceptor populations was dependent on whether the reflex was decreasing or increasing SNA. To address these issues, we have proposed a model to predict summation of sensory input from the baroreflex and the exercise pressor reflex (Fig. 5). The carotid baroreflex is considered an excitatory input signal to the CNS that increases SNA during muscle contraction despite the elevation in arterial blood pressure. However, for the baroreflex to function as an excitatory input it must first rapidly reset to a higher arterial pressure. Classic resetting of the carotid baroreflex during dynamic exercise has been demonstrated by Potts et al. (25) and Paplier and colleagues (22). Although the time course for baroreflex resetting has not been determined, several studies have shown that the cardiovascular responses during the initial onset of exercise were altered when pharmacologically induced changes in blood pressure were used to perturb the baroreflex (6, 29). In these studies, it was shown that, if the baroreceptor signal is considered an excitatory input, activation of both reflexes would produce a larger increase in SNA. This finding was supported by the present study. Because summing the individual blood pressure responses exceeded the response during coactivation, the net effect was that the carotid baroreflex and the exercise pressor reflex interacted in an occlusive manner. Thus this model illustrates that summation of a response produced by two separate reflex pathways cannot simply be added together to predict the response when both pathways are activated simultaneously. Furthermore, this study demonstrates that the interaction between two reflex systems that were mutually activated to increase sympathetic outflow was occlusive.
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Additive summation for HR control.
In the present study we reported an inhibitory interaction for the
reflex control of MAP. However, summation of the reflex tachycardia was
simply additive. That is, the combined effect of reflex activation on
the increase in MAP was only 66% of the summated response (80 vs. 106 mmHg; coactivation vs. summation, respectively), whereas summation of
the reflex tachycardia during combined activation was equal to the
summated HR response (26 vs. 26 beats/min, coactivation vs. summation,
respectively). A possible explanation for this finding may have been
the absence of parasympathetic control of the heart in this study.
Bilateral cervical vagotomy was performed to eliminate the reflex
buffering by both aortic and cardiopulmonary baroreceptors. If aortic
baroreceptors remained intact, the cardiovascular responses produced by
the carotid baroreflex and the exercise pressor reflex would have been
attenuated (28, 31, 35). Although vagotomy prevented vagally mediated
changes in HR, we felt that this would not affect the interaction
because it has been reported that -chloralose anesthesia virtually
eliminates vagal control of HR (4). Furthermore, it is
likely that complete expression of a chronotropic response requires
both withdrawal of vagal tone and an increase in cardiac SNA (20).
Therefore, in the absence of vagal control of HR reported in this
study, it is difficult to reconcile the additive summation between
these two reflex pathways.
Potential limitations of the study.
First, lack of complete surgical isolation of the carotid sinus regions
represents a potential problem in the interpretation of these findings.
We found that, accompanying the increase in blood pressure produced by
bilateral carotid occlusion and muscle contraction/stretch, the
pressure in the carotid sinus region also increased gradually during
this period. Therefore, the afferent signal from carotid baroreceptors
was not constant over the period of muscle contraction and this may
have influenced our results. However, the change in sinus pressure
during BCO was similar to that produced when carotid occlusion was
accompanied by muscle contraction or stretch (48 ± 7 mmHg vs. 55 ± 8 mmHg, baroreflex vs. coactivation, respectively,
t = 
0.745, df = 20, P = 0.465). Hence, the
increase in sinus pressure was equivalent during each perturbation, and
therefore, this effect likely contributed to a similar degree in
determining the integration between these two reflexes.
MAP 30 mmHg), which may have increased perfusion to the contracting hindlimb,
and, therefore, reduced the afferent "signal" from skeletal muscle by washing out the metabolic by-products that are known to
activate metabolically sensitive receptors (19). Electrically induced
muscle contraction has been reported to increase hindlimb blood flow
(35). However, Waldrop and Mitchell (35) found that blood flow to the
contracting hindlimb was not affected after acute baroreceptor
deafferentation that significantly increased the pressor response
during muscle contraction. Furthermore, the possibility that the
increase in blood pressure affected the integration of sensory input
from these two reflexes is unlikely because the interaction between the
baroreflex and activation of the exercise pressor reflex by passive
muscle stretch (a stimulus that does not alter skeletal muscle
perfusion or muscle oxygenation) was the same as the interaction that
resulted during electrically induced muscle contraction. Therefore, any
change in muscle blood flow that may have occurred during activation of
both reflexes was not a sufficient stimulus to alter the interaction
between the baroreflex and the exercise pressor reflex.
Finally, although single fiber recordings have shown that group III/IV
muscle afferents discharge during electrically induced muscle
contraction and passive stretch (11, 18), some group III/IV afferents
also exhibit nociceptive properties (12). At least a portion of these
muscle afferents are polymodal, thereby precluding precise
categorization of these fibers. Therefore, although the responses in
the present study are thought to have resulted from ergoreceptor
activation, we cannot rule out the possibility that some of these
responses may have been mediated by contraction- and stretched-induced
muscle nociceptors.
Summary. Findings from the present study demonstrate a central neural occlusive interaction between the carotid baroreflex and the exercise pressor reflex. When both reflexes were activated to increase sympathetic outflow, the reflex cardiovascular responses were attenuated 33% compared with when each reflex was activated separately and the responses summated. This result suggests an occlusive interaction between the exercise pressor reflex and the carotid baroreceptor reflex. Moreover, inhibition of sympathetic outflow occurred at site(s) located in the CNS and was not attributed simply to the inability of effector organs to generate increases in HR and blood pressure. However, within the constraints of the present study, summation of the chronotropic response was simply additive. This contrast in summation may be attributed to the absence of parasympathetic innervation of the heart and/or to differences in the central circuitry and descending efferent pathways that project to the heart and the peripheral vasculature.
In conclusion, these data indicate that reflex sympathoexcitation evoked by inhibition of the carotid baroreflex and activation of the exercise pressor reflex is integrated in an occlusive manner. A similar degree of inhibition was found between these two reflexes when muscle afferents were activated by either muscle contraction or passive stretch. This suggests that central integration of somatic input from mechanosensitive receptors (passive muscle stretch) and combined mechano- and metaboreceptors (electrically induced muscle contraction) is similar. The anatomic substrates and the electrophysiological/neurochemical mechanisms mediating the central neural occlusive interaction between arterial baroreceptors and the skeletal muscle receptors await further investigation.| |
ACKNOWLEDGEMENTS |
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The authors thank James Jones, Julius Lamar, Jr., and Brian Treuhaft for expert technical assistance as well as Dr. Jim Pawelczyk for the development of the asynchronous data-acquisition subroutines used for real-time data collection and post hoc analyses.
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FOOTNOTES |
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This work was supported by National Heart, Lung, and Blood Program Project Grant HL-06296 and the Lawson and Rogers Lacy Research Fund in Cardiovascular Disease.
Address for reprint requests: J. T. Potts, Dept. of Physiology, Harry S. Moss Heart Center, Univ. of Texas Southwestern Medical Center, 5323 Harry Hines Blvd. Dallas, TX 75235-9034.
Received 23 July 1997; accepted in final form 21 November 1997.
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Top
Abstract
Introduction
Methodology
Results
Discussion
References
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),
2) activation of carotid baroreceptors by bilateral carotid occlusion (
), and
3) activation of both reflexes
simultaneously (
). Brackets show periods of baroreflex and skeletal
muscle reactivation. Values are means ± SE. bpm, Beats/min.
* Significantly different from control, P < 0.05. 
Significant difference
between coactivation and activation of each reflex separately,
P < 0.05. Values are means ± SE.
Significantly
different from coactivation, P < 0.05. 
Significantly different from algebraic summation,
P < 0.05.
