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Am J Physiol Heart Circ Physiol 274: H1841-H1847, 1998;
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Vol. 274, Issue 5, H1841-H1847, May 1998

RAPID COMMUNICATION
Interaction between carotid baroreflex and exercise pressor reflex depends on baroreceptor afferent input

Jeffrey T. Potts and Jianhua Li

Departments of Physiology and Internal Medicine, Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, Texas 75235-9034

    ABSTRACT
Top
Abstract
Introduction
Methods
Results
Discussion
References

Because arterial baroreceptor and skeletal muscle receptor afferents project to cardiovascular regions in the lower brain stem such as the nucleus tractus solitarii (NTS), it is likely that the level of baroreceptor afferent input will modify the excitatory cardiovascular responses evoked by contraction-sensitive skeletal muscle afferents. The purpose of this study was to determine the effect of carotid sinus baroreceptor afferent input (CSA) on reflex heart rate (HR) and mean arterial pressure (MAP) responses evoked by activation of skeletal muscle receptor afferents (SMA). CSA input was servo controlled at three levels of carotid sinus pressure using the isolated carotid sinus preparation, and SMA input was varied by induced muscle contraction (L7-S1 ventral root stimulation) or passive muscle stretch. Experiments were performed in alpha -chloralose-anesthetized and vagotomized dogs (n = 9). When CSA input was low (106 ± 35 mmHg), electrically induced muscle contraction increased HR and MAP (30 ± 8 beats/min and 42 ± 12 mmHg, respectively, P < 0.05). However, when CSA input was high (221 ± 9 mmHg), the reflex changes in HR and MAP during muscle contraction were attenuated (6 ± 4 beats/min and 18 ± 4 mmHg, respectively, P < 0.05). Similarly, the sympathoexcitatory responses evoked by passive muscle stretch were attenuated in a baroreceptor-dependent manner. These results suggest that changing CSA input from low (106 mmHg) to high (221 mmHg) shifts the interaction from facilitation to inhibition. Therefore, it is concluded that the nature of the interaction (i.e., facilitation or inhibition) between the baroreflex and the exercise pressor reflex is dependent on the level of baroreceptor input. Moreover, our findings substantiate early studies showing that the level of afferent input from arterial baroreceptors is a powerful modulator of sympathoexcitation evoked by mechanically and metabolically sensitive skeletal muscle receptors.

skeletal muscle receptor afferent stimulation; nucleus tractus solitarii; ventrolateral medulla; cardiovascular-related neurons; cardiovascular pressor reflexes; exercise

    INTRODUCTION
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Abstract
Introduction
Methods
Results
Discussion
References

THE INTEGRATION of cardiovascular-related neural input signals during exercise is not completely understood. The cardiovascular response evoked during exercise is the outcome of a central interaction between three sources of neural input: 1) cortical activation of cardiovascular-related brain stem neurons (central command), 2) afferent input from contraction-sensitive skeletal muscle receptors (exercise pressor reflex), and 3) afferent input from arterial and cardiopulmonary baroreceptors. Afferent projections from two of these neural mechanisms, arterial baroreceptors and skeletal muscle receptors, synapse in discrete regions of the medulla that are related to cardiovascular function, such as the nucleus tractus solitarii (NTS) (6, 8, 14, 20). Therefore, it is likely that the level of baroreceptor afferent input will modify the excitatory cardiovascular response evoked by contraction-sensitive skeletal muscle receptors.

Because the arterial baroreceptor reflex is best characterized as possessing nonlinear behavior (i.e., variable gain with threshold and saturation plateaus), the location of the operating point on the baroreflex curve (i.e., steady-state relationship between heart rate and arterial blood pressure) will be essential to the nature of the interaction between the baroreflex and the exercise pressor reflex. Previously, we (23) demonstrated that the carotid baroreflex and the exercise pressor reflex interact in an inhibitory manner. Furthermore, we found that the site of inhibition was restricted to the central nervous system (CNS). However, because this interaction was only examined at a single point on the stimulus-response curve, it is not known whether changing the operating point of the baroreflex would alter the interaction between these two reflex pathways.

Therefore, the purpose of the present study was to determine the effect of varying the level of carotid sinus baroreceptor afferent input (CSA) on the reflex heart rate (HR) and mean arterial pressure (MAP) responses evoked by activation of skeletal muscle receptor afferents (SMA). The level of CSA input was altered using a servo-controlled and isolated carotid sinus preparation, and SMA input was varied by electrically induced muscle contraction (L7-S1 ventral root stimulation) and by passive stretch of the hindlimb in the dog. We hypothesized that when the baroreflex was close to its threshold pressure, the sympathoexcitatory response evoked by skeletal muscle receptors would be augmented (i.e., facilitatory interaction), whereas when the baroreflex was near its saturation pressure, sympathoexcitation would be attenuated (i.e., inhibitory interaction).

    METHODS
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Abstract
Introduction
Methods
Results
Discussion
References

Surgical preparation. Studies were conducted in nine alpha -chloralose-urethan-anesthetized dogs (10-15 kg). Induction of anesthesia was performed with thiopental sodium (10-12 mg/kg iv) and anesthesia was maintained with alpha -chloralose (80 mg/kg) and urethan (200 mg/kg). Supplemental anesthesia was administered every 90 min (alpha -chloralose, 15 mg/kg; urethan, 75 mg/kg) via a catheter in the femoral vein. An endotracheal tube was inserted and connected to a piston-type respirator (model 613, Harvard) set at 20 ml/kg tidal volume and respiratory frequency of 15-20 min-1. The animals were ventilated with room air, and the adequacy of ventilation was determined from arterial blood gas measurements (ABL3 Acid Base Laboratory, Radiometer, Copenhagen, Denmark) obtained every ~30-45 min. Arterial PO2 and PCO2 were kept within normal limits by enriching the inspired O2 supply and adjusting the ventilatory rate or volume. In cases of metabolic acidosis, sodium bicarbonate (8.4% solution) was infused to maintain an arterial blood pH of ~7.4 ± 0.05. Body temperature was monitored with a rectal probe and was maintained at 38.0 ± 0.5°C with a water-perfused heating pad and a near-infrared heating lamp.

The left and right carotid sinuses were vascularly isolated from the remainder of the circulation and were perfused with varied levels of static pressure. Briefly, the internal and external carotid arteries and any small branches originating from the carotid bifurcation were completely ligated. The occipital arteries were ligated at their origin to eliminate blood flow to the carotid chemoreceptor body. The lingual arteries were cannulated and connected to a pressure transducer (Statham P23 Db) for the measurement of carotid sinus pressure (CSP). The left and right common carotid arteries were cannulated proximal to the carotid bifurcation with a three-way connector, and the free end of the connector was attached to a servo-controlled, nonpulsatile pressure-generating system. In addition, the left common carotid artery was cannulated with polyvinyl chloride tubing (ID 0.059 in., OD 0.128 in.) and advanced to the junction of the brachiocephalic artery and the aorta for the measurement of systemic arterial pressure (SAP). All pressure transducers were calibrated with known reference pressures before and after each experiment. The perfusate used in the extracorporeal circuit (lactated Ringer, Baxter) was buffered to pH 7.4 and equilibrated with 95% O2-5% CO2. Because the extracorporeal circuit was not a follow-through system, the perfusate was exchanged with new stock every 60 min to aid in maintaining the desired PO2, PCO2, and pH in the carotid sinus regions. This was achieved by opening the lingual arterial cannula for 30 s to permit new perfusate to flow into the sinus regions. The vagosympathetic trunks were tied and cut bilaterally proximal to the carotid bifurcation to eliminate buffering from the aortic and cardiopulmonary baroreceptors.

A limited laminectomy was performed to expose the spinal cord at the level of the lower lumbar-upper sacral region. Care was taken to remove only those vertebrae necessary to expose the dorsal and ventral spinal rootlets at the L7 and S1 levels. The dog was positioned into a head and spinal unit (David Kopf Instruments, Tujunga, CA), and the pelvis was secured with stabilizing pins. The dura was opened longitudinally, and the L7 and S1 spinal roots were identified. The ventral roots were carefully dissected from the dorsal roots, sectioned, and placed on bipolar platinum stimulating electrodes. The stimulating electrodes were covered in a pool of warmed mineral oil (37°C) and connected to a high-impedance signal isolation unit (model F-HIP511G, Grass Instruments, Quincy, MA) and a stimulator (model S88, Grass Instruments). The skin covering the ipsilateral lower limb was removed, the calcaneal bone was sectioned, and the Achilles tendon was connected to a force transducer (model F10, Grass Instruments) to measure the amount of tension generated during electrically induced contraction and mechanical stretch of the gastrocnemius. Finally, the lower limb was stabilized by attaching the patellar tendon to a steel post. The completed instrumentation and the extracorporeal carotid sinus circuit are illustrated in Fig. 1.


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  		Fig. 1.   Schematic illustration of surgical instrumentation used to study interaction between carotid baroreceptors and skeletal muscle receptors. Shown is extracorporeal circuit that perfused carotid sinus regions to control level of baroreceptor afferent input (A) and ventral root preparation used to contract dog hindlimb (B).

All cardiovascular signals were recorded directly by an eight-channel physiological recorder (model 2800S, Gould Instruments). These signals were also sampled at 100 Hz by commercially available data acquisition software (Global Lab 3, Data Translation) and stored by a videotape multiplex adaptor (model 4000, Vetter) and recorder (model PV-4760, Panasonic) for later analyses.

Experimental protocol. After surgery was completed a period of 60 min was permitted for stabilization. CSP was set at either a low-, mid-, or high-pressure level (CSPLo, CSPMid, CSPHi, respectively), and activation of skeletal muscle afferents was performed by 1) electrical stimulation of L7 and S1 ventral roots at 3× motor threshold, a stimulus frequency of 30 Hz, and a pulse duration of 0.1 ms or 2) mechanical stretch of the hindlimb. Every attempt was made to match the level of muscle tension during passive stretch to the level of tension generated during electrically induced contraction. The reflex-evoked changes in HR and MAP were recorded continuously 30 s before activation of skeletal muscle receptors and during the period (1 min) of muscle contraction or stretch. The level of CSP (CSPLo, CSPMid, CSPHi) and the sequence muscle afferent activation (electrically induced muscle contraction or passive muscle stretch) were randomized. It was found that the order of presentation did not affect the reflex cardiovascular responses. Therefore, the data were combined and the effect of baroreceptor activation on the reflex cardiovascular responses evoked by skeletal muscle receptors was compared.

Statistical analyses. The reflex HR and MAP responses to the randomized sequence of CSP (CSPLo, CSPMid, CSPHi) and electrically induced muscle contraction or passive muscle stretch were grouped accordingly and averaged. The sympathetically mediated cardiovascular responses produced by electrically induced muscle contraction or passive muscle stretch at each level of baroreceptor activity were compared by analysis of variance and post hoc by Student-Newman-Keuls test. Data are presented as means ± SD. Significant difference was determined as P < 0.05.

    RESULTS
Top
Abstract
Introduction
Methods
Results
Discussion
References

An example of the effect of varying the level of carotid baroreceptor input on the reflex hemodynamic responses evoked by electrically induced contraction of the gastrocnemius is shown in Fig. 2. When CSP was controlled at ~75 mmHg, the baseline HR and MAP were 200 beats/min and 125 mmHg, respectively. Ventral root stimulation generated ~6 kg of muscle tension that produced a 25% increase in HR (200 right-arrow 250 beats/min) and a 52% increase in MAP (125 right-arrow 190 mmHg). When CSP was increased to ~200 mmHg, baseline HR and MAP were decreased (180 beats/min and 95 mmHg, respectively). Activation of contraction-sensitive skeletal muscle receptors by induced muscle contraction increased HR by only 6% (180 right-arrow 190 beats/min) and MAP by only 21% (95 right-arrow 115 mmHg).


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  		Fig. 2.   Example of reflex blood pressure (SAP) and heart rate (HR) responses evoked by electrically induced muscle contraction at 2 levels of carotid sinus pressure (CSP). Left: changes in SAP and HR when L7-S1 ventral roots were electrically stimulated and CSP was servo controlled at 75 mmHg. Right: contraction-induced increases in SAP and HR were attenuated when CSP was servo controlled at 200 mmHg. Note that blunting of contraction-induced responses by high baroreceptor input occurred despite greater level of generated muscle tension.

A summary of the effect of the carotid baroreceptor reflex on baseline hemodynamics and the reflex cardiovascular responses evoked by electrically induced muscle contraction and passive muscle stretch is shown in Table 1. When the afferent activity from carotid baroreceptors was increased from CSPLo (106 ± 35 mmHg) to CSPHi (221 ± 9 mmHg), baseline HR and MAP progressively decreased (P < 0.05). Electrically induced muscle contraction produced equivalent increases in hindlimb muscle tension irrespective of the level of carotid baroreceptor activity [5.1 ± 0.7 vs. 5.6 ± 0.4 vs. 5.3 ± 0.5 kg, CSPLo vs. CSPMid vs. CSPHi; P = not significant (NS)]. However, when CSP was servo controlled at CSPHi, the reflex increases in HR and MAP evoked by skeletal muscle contraction were attenuated (P < 0.05). A similar trend was found when muscle afferents were activated by mechanical stretch of the hindlimb (see Table 1). However, the reflex increases in HR and MAP caused by muscle contraction and stretch were never completely abolished when CSP was servo controlled at the highest level.

                              
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  		Table 1.   Effect of carotid baroreceptor reflex on baseline hemodynamics and reflex cardiovascular responses evoked by electrically induced muscle contraction and passive muscle stretch of dog hindlimb

The average changes in HR and MAP from baseline during electrically induced muscle contraction and mechanical stretch of the hindlimb at the three levels of CSP are shown in Fig. 3. There was no difference in the generated level of muscle tension by electrically induced contraction and mechanical stretch of the hindlimb during the three levels of CSP (P = NS). However, the tension development during mechanical stretch was significantly greater than the tension developed during electrically induced contraction (7.4 vs. 5.3 kg). Furthermore, there was no difference in each level of CSP (Lo, Mid, Hi) that was used to alter afferent baroreceptor activity during electrically induced muscle contraction and passive muscle stretch (P = NS).


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  		Fig. 3.   Grouped data of average change in HR (filled bars) and mean arterial pressure (MAP, open bars) from baseline during passive muscle stretch (A) and electrically induced muscle contraction (B) at 3 levels of carotid baroreceptor afferent activity (Lo, 97 ± 18 mmHg; Mid, 142 ± 14 mmHg; Hi, 219 ± 7 mmHg). * Significantly different from Lo level activity (P < 0.05).

    DISCUSSION
Top
Abstract
Introduction
Methods
Results
Discussion
References

The major new finding of the present study is that the nature of the interaction between the carotid baroreflex and the exercise pressor reflex (i.e., facilitation or inhibition) is determined by the level of baroreceptor input. Our results indicate that increasing the level of carotid baroreceptor afferent input (i.e., low to high) transforms the interaction from facilitation to inhibition. Although an inhibitory interaction between these two reflex pathways has been well documented (28, 34, 35), we have shown that facilitation of the sympathoexcitatory responses may also occur. Because vagotomy was used to eliminate afferent input from aortic and cardiopulmonary baroreceptors, the reflex cardiovascular responses evoked by these two reflex pathways were mediated exclusively by changes in sympathetic efferent motor activity. Therefore, the interaction described in this study is limited to the redundant control of sympathoexcitation by both the carotid baroreflex and the exercise pressor reflex.

The results from the present study are in general agreement with previous studies that showed that afferent input from arterial baroreceptors is a powerful modulator of sympathoexcitation evoked by activation of mechanically and metabolically sensitive skeletal muscle afferents. In a series of experiments by Donald, Walgenbach, and colleagues (10, 17, 35) the effect of neural input from aortic, cardiopulmonary, and carotid sinus baroreceptors on the cardiovascular responses during dynamic exercise was examined. Dogs were studied before and after surgical aortic arch denervation and acute interruption of carotid baroreceptor input by vascularly isolating the carotid sinuses (29). Barodenervation decreased baseline blood pressure but did not alter the response to exercise when carotid baroreceptors were close looped. However, after chronic aortic denervation and isolation of the carotid sinuses at a static pressure (open-loop condition), the increase in arterial pressure was significantly greater during exercise. The potentiated arterial blood pressure response was caused exclusively by regional vasoconstriction, because the cardiac output response was not altered. These data suggest that preventing the increase in afferent baroreceptor activity produced by the accompanying increase in blood pressure during exercise resulted in a greater sympathoexcitation and augmentation of the blood pressure response. Furthermore, because it has been shown that deafferentation of all baroreceptor populations results in a profound fall in arterial blood pressure after the onset of exercise (10, 17, 35), afferent input from arterial baroreceptors is necessary to elicit the typical cardiovascular responses evoked during exercise (i.e., reflex tachycardia and pressor response). The findings from the present study support this concept. Moreover, our findings indicate that the level of baroreceptor input is a powerful modulator of the sympathoexcitatory responses evoked by activation of skeletal muscle receptors during muscle contraction.

Different experimental approaches were previously employed to address this question in both animals and humans. DiCarlo and Bishop (12) showed that delaying the rise of arterial pressure at the onset of exercise by infusion of nitroglycerin markedly increased renal sympathetic nerve activity and heart rate in rabbits exercising on a treadmill. A similar approach was used by Scherrer et al. (26) in humans performing static handgrip exercise. In this study, sodium nitroprusside and phenylephrine were infused to control the level of arterial baroreceptor activity during isometric handgrip. It was found that the heart rate response, and the changes in muscle sympathetic nerve activity (recorded from the peroneal nerve) evoked by handgrip exercise, were potentiated ~300% during nitroprusside infusion and attenuated ~50% during phenylephrine infusion. Taken together, these findings from both animal and human studies suggest that afferent input from arterial baroreceptors is a modulator of sympathoexcitation during both dynamic and static forms of exercise.

The mechanisms responsible for baroreceptor-dependent modulation of sympathetic excitation during exercise, and the anatomic substrates involved, are currently under intense investigation. However, it is likely that this interaction occurs within central autonomic pathways (15). At least two possibilities exist: 1) modulation of GABAergic inhibition of sympathetic neurons in the rostral ventrolateral medulla (rVLM) and/or 2) altered transmission of primary baroreceptor input in NTS neurons. It is now well established that neurons in the rVLM with axons that project to the intermediolateral columns of the spinal cord are primarily responsible for the basal level of sympathetic nerve discharge (3, 7, 9, 13). These preganglionic sympathetic motor neurons receive modulatory inputs (excitatory and inhibitory inputs) from arterial baroreceptors, somatosensory receptors (nociceptive and nonnociceptive), and hypothalamic and cortical neurons (2, 4, 5, 25, 33). Bauer et al. (4, 5) identified neurons in the rVLM that increased their firing frequency when muscle afferents were activated by electrically induced muscle contraction. Moreover, these neurons were characterized as possessing a cardiac-related rhythm, suggesting that they may be involved in cardiorespiratory control (5, 19). In the context of the present study, facilitation of the discharge rate of excitatory preganglionic sympathetic rVLM neurons during contraction-induced activation of skeletal muscle receptors would be produced when afferent activity in the central baroreceptor pathways is low. Neurons in the rVLM receive tonic inhibitory input related to the level of afferent arterial baroreceptor input (1, 30). Generally, it is accepted that central baroreceptor pathways consist of an excitatory projection from the NTS to the caudal VLM (cVLM) (1) and an inhibitory GABAergic projection from the cVLM to the sympathetic preganglionic motor neurons in the rVLM (30). Because the neurotransmitter for the inhibitory projection from the cVLM to the rVLM is GABA, it follows that a reduction in GABA release will increase the activity of rVLM neurons and elevate the level of preganglionic sympathetic motor activity. This enhanced sympathoexcitation may explain the augmented reflex responses when baroreceptor afferent input to the NTS is low, as reported in this study. Therefore, modulation of rVLM neurons by the level of afferent input from arterial baroreceptors is one mechanism that may account for baroreceptor-dependent adjustments in sympathoexcitation.

Alternatively, the level of central sympathetic outflow may be altered by the degree of convergence of neural input from arterial baroreceptors and contraction-sensitive skeletal muscle receptors via an alteration in the transmission of afferent baroreceptor input in the NTS. NTS neurons are targets for both arterial baroreceptor and skeletal muscle receptor afferent projections, and they are activated by synaptic input from both arterial baroreceptors and skeletal muscle receptors (22, 27, 31, 32). Although the NTS is primarily known as the site of central termination of primary baroreceptor afferents (8, 11), neuroanatomic studies by Kalia et al. (14) and Nyberg and Blomqvist (20) have reported that ascending neurons from skeletal muscle and the lumbar-sacral spinal cord also project to the NTS. Furthermore, Person (22), McMahon et al. (16), Toney and Mifflin (31, 32), and Seagard et al. (27) have provided electrophysiological evidence that NTS neurons are activated and/or inhibited during somatic and baroreceptor stimulation. Moreover, it has been proposed that the discharge characteristics of NTS neurons can be altered when sensory inputs from two or more visceral inputs converge on to the same NTS cell (18). Such an alteration in discharge patterns of neurons, referred to as time-dependent inhibition (18), has been suggested to modulate baroreflex function at the first synapse in the central baroreflex pathway (31, 32). Therefore, time-dependent inhibition of NTS neuronal responses represents a second mechanism that may be involved in the integration of cardiovascular-related inputs from skeletal muscle and arterial baroreceptors during physical activity or exercise.

Perspectives. The present data suggest that summation of sympathoexcitation between the baroreflex and the exercise pressor reflex can be either inhibitory or facilitatory and that the nature of the summation is determined by the level of neural input from arterial baroreceptors. The arterial baroreceptor reflex has classically been considered a negative-feedback controller that tonically inhibits the sympathetic neural motor responses evoked by the exercise pressor reflex (28, 34). However, it was recently proven that the carotid baroreflex is reset to a higher arterial blood pressure during dynamic exercise with no change in reflex sensitivity or gain (21, 24). Potts et al. (24) proposed that the functional significance for baroreflex resetting was to buffer the elevation in systemic blood pressure that was evoked by the exercise pressor reflex during moderate-to-severe intensities of exercise. DiCarlo and Bishop (12) also suggested that resetting of the arterial baroreflex supports the increase in arterial pressure at the onset of exercise rather than opposing it. Because baroreflex resetting must be accompanied by an increase in the set point of the baroreceptor stimulus-response relationship, it follows that acute resetting would render the baroreflex an "input stimulus" that raises sympathetic neural activity at the onset of exercise. Therefore, the baroreflex likely plays two functional roles in the regulation of arterial blood pressure during exercise, i.e., in addition to buffering the degree of sympathoexcitation evoked during moderate-to-severe intensities of exercise, the baroreflex also increases sympathoexcitation at the onset of exercise to minimize the initial fall in arterial blood pressure.

In the context of a physiological stressor such as exercise, the findings from the present study describing the interaction between the baroreflex and the exercise pressor reflex may be interpreted as follows. At exercise onset, rapid resetting of the arterial baroreflex (which decreases the functional level of afferent baroreceptor input to the CNS) facilitates the sympathoexcitatory responses evoked by the exercise pressor reflex. Thus, at exercise onset, these two reflexes interact synergistically to increase sympathoexcitation to minimize the transient fall in blood pressure and hypoperfusion of active skeletal muscle. However, during a moderate-to-severe intensity of exercise that elevates arterial blood pressure and the level of afferent baroreceptor input to the CNS, the magnitude of sympathoexcitation evoked by the exercise pressor reflex is attenuated. Therefore, during a high intensity of exercise these two reflexes interact in an inhibitory manner. We are currently using extracellular single-unit recordings to determine the electrophysiological basis for the interaction between the baroreflex and the exercise pressor reflex, i.e., the shift from a synergistic interaction at exercise onset to an inhibitory interaction during moderate-to-severe exercise intensities. This intriguing association between the baroreflex and the exercise pressor reflex and its physiological implications should be the subjects of future investigations.

In summary, the level of afferent activity from carotid baroreceptors plays a crucial role in determining the magnitude of the excitatory sympathetic responses evoked by skeletal muscle mechanoreceptors and metaboreceptors. We found that a low level of baroreceptor input facilitated the sympathoexcitatory response mediated by mechanosensitive and metabosensitive skeletal muscle receptors (i.e., facilitatory interaction), whereas a high level of afferent baroreceptor input attenuated these responses (i.e., inhibitory interaction). This type of association between the baroreceptor reflex and the exercise pressor reflex suggests that the interaction is not static but that it is dynamic. Moreover, these data suggest that the magnitude of inhibition or facilitation depends on the level of baroreceptor afferent input to the central nervous system. We speculate that this interaction is mediated, in part, by alterations in synaptic transmission in medullary regions that receive both arterial baroreceptor and skeletal muscle receptor afferents. These regions include, but are not limited to, the NTS and the VLM. Furthermore, it is suggested that the NTS represents the first central site in which both arterial baroreceptor and somatosensory receptor afferent signals may be processed. Therefore, it is proposed that in addition to the well-recognized role of preganglionic sympathetic motor neurons in the rVLM, the NTS also represents a central integrating site for cardiovascular-related neural signals during exercise. The electrophysiological mechanisms, as well as the neurochemical substances, involved in the processing of sensory input by NTS neurons await further investigation.

    ACKNOWLEDGEMENTS

The authors acknowledge the excellent technical assistance of James Jones, Julius Lamar, Jr., and Margaret Robledo. The authors also express gratitude to Dr. Jere H. Mitchell for generous support and encouragement in this study.

    FOOTNOTES

This work was supported by American Heart Association-Texas Affiliate Grant 97G-101 awarded to J. T. Potts.

Address for reprint requests: J. T. Potts, Dept. of Physiology, Harry S. Moss Heart Ctr., Univ. of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75235-9034 (E-mail: jpotts{at}mednet.swmed.edu).

Received 9 December 1997; accepted in final form 18 February 1998.

    REFERENCES
Top
Abstract
Introduction
Methods
Results
Discussion
References

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AJP Heart Circ Physiol 274(5):H1841-H1847
0363-6135/98 $5.00 Copyright © 1998 the American Physiological Society


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