HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) All Versions of this Article: 289/4/H1604    most recent 00053.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Yamamoto, K. Articles by Sunagawa, K. Search for Related Content PubMed PubMed Citation Articles by Yamamoto, K. Articles by Sunagawa, K.

Static interaction between muscle mechanoreflex and arterial baroreflex in determining efferent sympathetic nerve activity

¹Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka; ²Pharmaceuticals and Medical Devices Agency, Tokyo; and ³Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan

Submitted 18 January 2005 ; accepted in final form 13 May 2005

	ABSTRACT

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION GRANTS REFERENCES

 
Elucidation of the interaction between the muscle mechanoreflex and the arterial baroreflex is essential for better understanding of sympathetic regulation during exercise. We characterized the effects of these two reflexes on sympathetic nerve activity (SNA) in anesthetized rabbits (n = 7). Under open-loop baroreflex conditions, we recorded renal SNA at carotid sinus pressure (CSP) of 40, 80, 120, or 160 mmHg while passively stretching the hindlimb muscle at muscle tension (MT) of 0, 2, 4, or 6 kg. The MT-SNA relationship at CSP of 40 mmHg approximated a straight line. Increase in CSP from 40 to 120 and 160 mmHg shifted the MT-SNA relationship downward and reduced the response range (the difference between maximum and minimum SNA) to 43 ± 10% and 19 ± 6%, respectively (P < 0.01). The CSP-SNA relationship at MT of 0 kg approximated a sigmoid curve. Increase in MT from 0 to 2, 4, and 6 kg shifted the CSP-SNA relationship upward and extended the response range to 133 ± 8%, 156 ± 14%, and 178 ± 15%, respectively (P < 0.01). A model of algebraic summation, i.e., parallel shift, with a threshold of SNA functionally reproduced the interaction of the two reflexes (y = 1.00x – 0.01; r² = 0.991, root mean square = 2.6% between estimated and measured SNA). In conclusion, the response ranges of SNA to baroreceptor and muscle mechanoreceptor input changed in a manner that could be explained by a parallel shift with threshold.

muscle stretch; exercise pressor reflex; exercise; subliminal fringe

Recent studies (13, 26) demonstrated that treadmill exercise or the muscle mechanoreflex extends the response range of SNA (i.e., the difference between maximum and minimum SNA) in the arterial baroreflex. The extension of the response range was mainly attributed to an increase in maximum SNA but not to changes in minimum SNA. On the other hand, Potts and Li (16) showed that higher carotid sinus pressure (CSP) attenuates the pressor response induced by the muscle mechanoreflex compared with lower CSP. We therefore hypothesized that the response range of SNA to either the muscle mechanoreflex or the arterial baroreflex would be changed depending on the afferent inputs from the other reflex.

To test the above-described hypothesis, we examined the static SNA responses to a combination of a wide range of inputs (4 different levels of baroreceptor input and 4 different levels of muscle mechanoreceptor input) in anesthetized rabbits. The results indicated that the response ranges of SNA to baroreceptor and muscle mechanoreceptor input can change depending on the input from the other reflex.

	MATERIALS AND METHODS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION GRANTS REFERENCES

 
Surgical preparations. Animals were cared for in strict accordance with the "Guiding Principles for the Care and Use of Animals in the Field of Physiological Sciences" approved by the Physiological Society of Japan. All protocols were approved by the Animal Subjects Committee of the National Cardiovascular Center. Seven Japanese White rabbits weighing 2.6–3.0 kg were anesthetized via intravenous injection (2 ml/kg) of a mixture of urethane (250 mg/ml) and -chloralose (40 mg/ml) and were mechanically ventilated with oxygen-enriched room air. Supplemental anesthetics (0.2–0.3 ml·kg^–1·h^–1) were administered continuously to maintain stable AP and heart rate levels during intervals of experimental protocols, which were indicative of an appropriate level of anesthesia. Arterial blood was sampled from the left common carotid artery. The rabbits were slightly hyperventilated to suppress chemoreflexes (arterial PCO₂ ranged from 30 to 35 mmHg, arterial PO₂ > 300 mmHg). Arterial blood pH was within the physiological range when examined at the end of surgical preparation, as well as at the end of the experiment. The body temperature of each animal was maintained at 38°C with a heating pad. AP was measured with a high-fidelity pressure transducer (Millar Instruments, Houston, TX) inserted from the right femoral artery.

We isolated bilateral carotid sinuses from the systemic circulation by ligating the internal and external carotid arteries and other small branches originating from the carotid sinus region. The isolated carotid sinuses were filled with warmed physiological saline via catheters inserted through the common carotid arteries. CSP was controlled by a servo-controlled piston pump (model ET-126A, Labworks, Costa Mesa, CA). Bilateral vagal and aortic depressor nerves were sectioned at the neck to minimize reflexes from the cardiopulmonary region and from the aortic arch.

We exposed the left renal sympathetic nerve retroperitoneally and attached a pair of stainless steel wire electrodes (Bioflex wire AS633, Cooner Wire) to record SNA. The nerve bundle peripheral to the electrodes was tightly ligated and crushed to eliminate afferent signals from the kidney. The nerve and electrodes were secured with silicone glue (Kwik-Sil, World Precision Instruments, Sarasota, FL). The preamplified nerve signal was band-pass filtered at 150–1,000 Hz, full-wave rectified, and low-pass filtered with a cutoff frequency of 30 Hz to quantify the nerve activity. Pancuronium bromide (0.1 mg/kg) was administered to prevent muscular activity from contaminating the SNA recordings.

With the rabbit in the prone position, the sacrum, left ankle, and knee were clamped with a custom-made apparatus to prevent body trunk and hindlimb movement during muscle stretch. The left triceps surae muscle, Achilles tendon, and calcaneus bone were exposed. The left triceps surae muscle was isolated from surrounding tissue. The Achilles tendon was severed from the calcaneus bone and attached to a force transducer (Load Cell LUR-A-SA1, Kyowa Electronic Instruments, Tokyo, Japan). During muscle stretch, the other side of the force transducer was connected to a weight via a pulley; muscle tension (MT) was quantified with this force transducer.

Protocols. We measured the steady-state SNA response to a number of combinations of CSP and MT as follows. CSP was initially decreased to 40 mmHg. After attainment of a steady state, CSP was increased from 40 to 160 mmHg in increments of 40 mmHg. Each pressure step was maintained for 120 s. Passive muscle stretch was applied during the last 60 s of each CSP step to develop MT. We repeated the stepwise CSP input four times while varying MT by 0, 2, 4, and 6 kg in random orders.

Data analysis. We recorded CSP, MT, SNA, and AP at a sampling rate of 200 Hz with a 12-bit analog-to-digital converter. Data were stored on a dedicated laboratory computer system for later analyses.

We calculated mean SNA and AP during the last 10 s of each CSP step. Because the absolute magnitude of SNA depended on recording conditions, SNA was presented in arbitrary units (a.u.) so that the minimum and maximum values of SNA data during the stepwise CSP input under 0-kg MT became 0 and 100 a.u., respectively, for each animal. We calculated the response range of SNA (the difference between maximum and minimum SNA) to the carotid sinus baroreflex based on the CSP-SNA relationship obtained at each MT level. We also calculated the response range of SNA to the muscle mechanoreflex based on the MT-SNA relationship obtained at each CSP level.

Statistical analysis. All data are presented as means ± SE. Differences were considered significant when P < 0.05. The effects of CSP and MT on SNA were tested by two-way ANOVA with repeated measurements. The response range of SNA in the CSP-SNA relationship or in the MT-SNA relationship was compared by one-way ANOVA with repeated measurements. In the case of a significant F-value, a post hoc test with the Newman-Keuls method was used to identify significant differences between any two of the conditions.

	RESULTS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION GRANTS REFERENCES

 
Figure 1 shows a typical time series of CSP, MT, SNA, and AP obtained from one animal. Although the panels are arranged in Fig. 1 in increasing order of MT, the MT levels were applied randomly in the experiments. SNA and AP decreased in response to the increments in CSP with all MT levels. SNA and AP increased in response to the increments in MT at CSP below 120 mmHg in this animal.

View larger version (24K): [in this window] [in a new window]   Fig. 1. Typical time series of intracarotid sinus pressure (CSP), muscle tension (MT), sympathetic nerve activity [SNA; in arbitrary units (a.u.)], and arterial pressure (AP) obtained from 1 animal. The 4 panels correspond to MT of 0, 2, 4, and 6 kg, in that order. SNA and AP decreased in response to increments in CSP at all MT levels. SNA and AP increased in response to the increments in MT at CSP below 120 mmHg in this animal. Data were resampled at 10 Hz.

View larger version (18K): [in this window] [in a new window]   Fig. 2. Muscle mechanoreflex at each CSP level (A) and carotid sinus baroreflex at each MT level (B). In the MT-SNA relationship (A), SNA proportionally increased in response to increments in MT at CSP of 40 and 80 mmHg. However, SNA did not increase except at MT of 6 kg at CSP of 120 mmHg and did not change at any MT level at CSP of 160 mmHg. In the CSP-SNA relationship (B), SNA decreased in response to increments in CSP at all MT levels. Two-way ANOVA indicated that there was a significant interaction between CSP and MT in determining SNA (P < 0.001). *P < 0.05 compared with MT of 0 kg at each CSP in the muscle mechanoreflex (A) and compared with CSP of 40 mmHg at each MT in the carotid sinus baroreflex (B).

Two-way ANOVA indicated a significant interaction between MT and CSP in determining SNA (P < 0.001), suggesting that the effects of the muscle mechanoreflex and the arterial baroreflex could not be explained by algebraic summation (15, 16).

The response range of SNA to the muscle mechanoreflex obtained at each CSP level is shown in Fig. 3A. The response range of SNA was significantly smaller at CSP of 120 and 160 mmHg than at CSP of 40 mmHg.

View larger version (13K): [in this window] [in a new window]   Fig. 3. Response range of SNA to the muscle mechanoreflex (A) and to the carotid sinus baroreflex (B). The response range to the muscle mechanoreflex (A) was smaller at CSP of 120 and 160 mmHg than at CSP of 40 mmHg. The response range to the carotid sinus baroreflex (B) was greater at MT of 2, 4, and 6 kg than at MT of 0 kg. *P < 0.05 compared with CSP of 40 mmHg in the muscle mechanoreflex (A) and compared with MT of 0 kg in the carotid sinus baroreflex (B).

Figure 4 illustrates the relationship between SNA and AP obtained by 16 combinations of 4 levels of CSP and 4 levels of MT. The relationship between SNA and AP can be characterized by a single sigmoid curve, indicating that the relationship between SNA and AP does not differ between the muscle mechanoreflex and the carotid sinus baroreflex.

View larger version (10K): [in this window] [in a new window]   Fig. 4. Relationship between SNA and AP obtained by 16 combinations of 4 levels of CSP and 4 levels of MT. The relationship between SNA and AP can be characterized by a single sigmoid curve, indicating that the SNA-AP relationship did not differ between the muscle mechanoreflex and the carotid sinus baroreflex.

	DISCUSSION

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION GRANTS REFERENCES

Interaction between muscle mechanoreflex and arterial baroreflex. We determined the maximum MT based on a preliminary study in which the SNA response to MT did not saturate at 6 kg. The accurate range for MT to mimic the physiological activation of muscle mechanoreceptor afferents was unclear. The maximum MT in the present study was threefold as strong as that which could occur if the configuration of Achilles tendon and calcaneus bone was kept intact (23). Although the maximum MT of 6 kg was nonphysiological and might have recruited nociceptive or nonspecific fiber activation, the SNA increased linearly with MT at CSP of 40 and 80 mmHg (Fig. 2A). Accordingly, the transition of physiological nonnociceptive stimulation to nonphysiological nociceptive stimulation was not clearly determined in the present experimental settings. The muscle mechanoreflex is mediated by group III and IV afferents (10, 12). The proportion of contraction-sensitive units with presumably mechanical mechanism of activation is higher among group III than group IV afferents (7). Discharge of group IV afferents is enhanced when the muscle is made ischemic. The dominant fiber type might have changed when the stimulation changed from nonnociceptive to nociceptive. Another concern is that because nociceptive stimulation of muscle afferents by metabolic products of contraction is likely to be related to exercise but stimulation by nonphysiological levels of stretch is not, the physiological significance of the present results should be interpreted carefully.

The effect of baroreceptor input on muscle mechanoreflex control of SNA has never been analyzed quantitatively over a wide range of inputs. SNA proportionally increased in response to increments in MT at CSP of 40 and 80 mmHg (Fig. 2A). However, SNA did not increase at CSP of 120 mmHg until MT of 6 kg was applied (Fig. 2A). As a result, the response range of SNA to MT was reduced by an increase in CSP (Fig. 3A). These data suggest that greater tension development above a certain level is necessary to evoke sympathoexcitation by the muscle mechanoreflex at higher CSP. Stebbins et al. (23) demonstrated that mean AP increased with increasing passive muscle stretch up to 8 kg, which suggests the SNA increase during passive muscle stretch. However, the AP response to passive muscle stretch might be modified by the accompanying arterial baroreflex in their study, because they did not open the arterial baroreflex negative-feedback loop. Potts and Li (16) demonstrated that higher CSP attenuated the sympathoexcitatory responses induced by muscle mechanoreflex. The present study extended the results by Potts and Li (16) by directly measuring SNA over a wide range of mechanoreceptor and baroreceptor inputs.

Elevation of MT increased the response range of SNA to CSP to 130%, 160%, and 180% at MT of 2, 4, and 6 kg, respectively, relative to that observed under MT of 0 kg (Fig. 3B). These results are consistent with results by Miki et al. (13), who demonstrated that treadmill exercise increases the response range of SNA in the arterial baroreflex. Muscle mechanoreflex may contribute to the extended response range of SNA in the arterial baroreflex during exercise. The pressor response was observed during tetanic contraction of the hindlimb induced by femoral nerve stimulation at 100 Hz in anesthetized and baroreceptor-deafferentiated rabbits (24). The static contraction also induces the pressor response in decerebrated rabbits (25). However, rhythmic contraction of the hindlimb by 3-Hz stimulation of the femoral nerve decreases mean AP (24). Both pressor and depressor responses were initiated from the contracting limbs, as both responses were eliminated after sectioning of the somatic nerves. To what extent the opposing reflexes participate in the regulation of SNA and AP during exercise awaits further investigation.

Our data are the first to demonstrate that sympathoexcitation induced by the muscle mechanoreflex requires development of a strong tension when CSP is high. On the other hand, weak tension development is sufficient to evoke sympathoexcitation at a lower CSP, possibly antagonizing a further reduction in AP during exercise (1, 16). An increased response range of SNA to CSP by muscle mechanoreceptor activation may also improve the pressure-stabilizing capacity of the arterial baroreflex against larger pressure disturbances such as those occurring during exercise (26). Furthermore, the muscle mechanoreflex and the carotid sinus baroreflex share a common output variable of SNA with regard to the regulation of AP, because the SNA-AP relationship cannot be discriminated between MT and CSP perturbations (Fig. 4). Together, these findings suggest that interaction of the two reflexes is beneficial to compensate for AP decreases resulting from exercise-induced vasodilation while maintaining the stabilization of AP against pressure disturbances.

Functional model for interaction between muscle mechanoreflex and carotid sinus baroreflex. A functional model of a given system is useful for understanding the physiological system through a simulation study. One can examine the performance of a given physiological system by simulating what would happen if the parameters of the model deviated from their normal physiological values. For instance, we have reported (8) the importance of high-cut baroreflex neural arc transfer characteristics in AP regulation by removing the high-cut characteristics in the simulation. Another application of a functional model is that it can provide a basis for development of an artificial device to support or replace the impaired physiological system. For instance, we have identified dynamic characteristics of the arterial baroreflex system and developed a framework of an artificial baroreflex center that can replace the failed vasomotor center (20, 21, 27). Currently, the artificial baroreflex center does not take account of any interactions from afferent inputs other than the baroreceptors. Quantitative analysis of interaction between the mechanoreflex and the arterial baroreflex is the first step toward the future improvement of the artificial baroreflex center, when the artificial baroreflex center will be able to adjust its function during exercise.

We constructed a functional model to reproduce the interaction between the muscle mechanoreflex and the carotid sinus baroreflex. The CSP-SNA relationship has been modeled by a sigmoid curve as follows (9):

(1)

where SNA_B is SNA derived from the baroreflex, P₁ denotes the response range (i.e., the difference between the maximum and minimum values of SNA), P₂ is the coefficient of gain, P₃ is the midpoint of the logistic function on the CSP axis, and P₄ is the minimum value of SNA.

The MT-SNA relationship can be modeled by a linear function as follows:

(2)

where SNA_M is SNA derived from the mechanoreflex, and A₁ and A₂ represent the slope and intercept, respectively. The linear model was based on the MT-SNA relationship at CSP of 40 and 80 mmHg (Fig. 2A).

We then constructed an integrative model from the above two models. We first constructed an algebraic summation model based on the MT-SNA relationship, which showed a parallel shift between CSP of 40 and 80 mmHg. To remove apparent changes in parameters in Eq. 1 for different MT and nonlinearity observed in the MT-SNA relationship for higher CSP, we introduced threshold in the summation model as follows:

(3)

where Th is a threshold value for SNA. The function max(a, b) gives the greater or equal value between a and b.

Figure 5 illustrates a hypothetical interaction between the muscle mechanoreflex and the arterial baroreflex in a model of algebraic summation with threshold (Eq. 3). Figure 5A is a simplified block diagram of the functional integration of two reflexes. The SNA control signals derived from the muscle mechanoreflex and the arterial baroreflex are summed, and then SNA is evoked if the sum exceeds a threshold Th. In the muscle mechanoreflex analysis (Fig. 5B), the increase in CSP input induces a parallel downward shift in the MT-SNA relationship from the solid thin line to the dashed line. Because of the threshold, SNA does not respond up to 4 kg of MT, resulting in the MT-SNA relationship shown by the solid thick line in Fig. 5B. In the arterial baroreflex analysis (Fig. 5C), the increase in MT input induces a parallel upward shift in the CSP-SNA relationship from the dashed line to the solid thick line. The observed CSP-SNA relationship at a low MT is shown as the solid thin line rather than the dashed line in Fig. 5C because of the threshold for SNA. Because of the subliminal fringe (gray area in Fig. 5, B and C), the response ranges of SNA for the muscle mechanoreflex and the arterial baroreflex can change depending on the input of the other reflex.

View larger version (18K): [in this window] [in a new window]   Fig. 5. Hypothetical model of interaction between the muscle mechanoreflex and the arterial baroreflex. A: simplified block diagram showing how the muscle mechanoreflex and the arterial baroreflex are functionally integrated based on the model of algebraic summation with a threshold (Th) (see Functional model for interaction between muscle mechanoreflex and carotid sinus baroreflex in DISCUSSIONfor details). NM and NB, neural arc subsystems for the muscle mechanoreflex and the arterial baroreflex, respectively. The signals derived from the muscle mechanoreflex and arterial baroreflex compartments were summed, and then the sum was compared with Th to yield SNA. B: muscle mechanoreflex. The increase in CSP input induces a parallel downward shift of the MT-SNA relationship from the solid thin line to the dashed line. SNA does not respond up to 4 kg of MT because of the threshold for SNA (solid thick line). C: arterial baroreflex. The increase in MT input induces a parallel upward shift in the CSP-SNA relationship from the dashed line to the solid thick line. The CSP-SNA relationship at a low MT would follow the solid thin line because of the threshold for SNA.

View larger version (31K): [in this window] [in a new window]   Fig. 6. A: averaged surface depicting the interaction between the muscle mechanoreflex and the carotid sinus baroreflex in determining SNA. B: surface depicting interaction, estimated by a model of algebraic summation, between the muscle mechanoreflex and the carotid sinus baroreflex with a SNA threshold. C: relationship between SNA estimated from the model and SNA actually measured. Each animal provided 16 data points (112 data points in total). The SNA estimated by the model was similar to the measured SNA. RMS, root mean square. Mean parameter values from Eq. 3 least-squares fitting on SNA data are as follows: P1, 193 a.u.; P2, 0.10 a.u./mmHg; P3, 101 mmHg; P4, –54 mmHg; A1, 15 a.u./kg; A2, –36 a.u.; Th, 3.0 a.u., where P1 is difference between maximum and minimum SNA; P2 is coefficient of gain; P3 is midpoint of logistic function on CSP axis, P4 is SNA minimum; A1 is slope; A2 is intercept; and Th is SNA threshold.

Second, we only focused on the static interaction and did not investigate the dynamic interaction between the muscle mechanoreflex and the arterial baroreflex in the present study. Further investigations focusing on the dynamic interaction are required.

Third, stretch of skeletal muscle provides a stimulus for activation of mechanoreceptors that is different from that which occurs during muscle contraction. During contraction, mechanoreceptors are activated by a shortening of skeletal muscle and by compression of the receptors. Thus mechanoreceptors may be stimulated in a very different manner during stretch, which would likely affect the magnitude of the corresponding reflex response. In addition, stretch may activate different afferents than contraction. Further studies are required to elucidate the interactions between baroreflex and muscle mechanoreflex induced by different modes of activation.

In conclusion, activation of afferents from baroreceptors shifted the MT-SNA relationship downward and reduced the response range. The activation of mechanosensitive afferents from skeletal muscles shifted the CSP-SNA relationship upward and extended the response range. A model of algebraic summation with a threshold may explain the integration of the two reflexes. The existence of the subliminal fringe may increase the capacity of the arterial baroreflex to stabilize AP during exercise and express the sympathoexcitatory responses induced by weak muscle mechanoreceptor input at lower AP.

	GRANTS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION GRANTS REFERENCES

 
This study was supported by a Health and Labour Sciences Research Grant for Research on Advanced Medical Technology from the Ministry of Health, Labour and Welfare of Japan (H14-Nano-002), by a Grant-in-Aid for Scientific Research (A) (15200040) from the Japan Society for the Promotion of Science, and by the Program for Promotion of Fundamental Studies in Health Science of the Pharmaceuticals and Medical Devices Agency of Japan.

	FOOTNOTES

 

Address for reprint requests and other correspondence: K. Yamamoto, Dept. of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan (e-mail: kentay{at}ri.ncvc.go.jp)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

	REFERENCES

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION GRANTS REFERENCES

 

1. DiCarlo SE and Bishop VS. Onset of exercise shifts operating point of arterial baroreflex to higher pressures. Am J Physiol Heart Circ Physiol 262: H303–H307, 1992.
2. Gallagher KM, Fadel PJ, Stromstad M, Ide K, Smith SA, Querry RG, Raven PB, and Secher NH. Effects of exercise pressor reflex activation on carotid baroreflex function during exercise in humans. J Physiol 533: 871–880, 2001.
3. Gallagher KM, Fadel PJ, Stromstad M, Ide K, Smith SA, Querry RG, Raven PB, and Secher NH. Effects of partial neuromuscular blockade on carotid baroreflex function during exercise in humans. J Physiol 533: 861–870, 2001.
4. Hayes SG and Kaufman MP. MLR stimulation and exercise pressor reflex activate different renal sympathetic fibers in decerebrate cats. J Appl Physiol 92: 1628–1634, 2002.
5. Ichinose M, Saito M, Wada H, Kitano A, Kondo N, and Nishiyasu T. Modulation of arterial baroreflex dynamic response during muscle metaboreflex activation in humans. J Physiol 544: 939–948, 2002.
6. Iellamo F, Legramante JM, Raimondi G, and Peruzzi G. Baroreflex control of sinus node during dynamic exercise in humans: effects of central command and muscle reflexes. Am J Physiol Heart Circ Physiol 272: H1157–H1164, 1997.
7. Kaufman MP, Longhurst JC, Rybicki KJ, Wallach JH, and Mitchell JH. Effects of static muscular contraction on impulse activity of groups III and IV afferents in cats. J Appl Physiol 55: 105–112, 1983.
8. Kawada T, Zheng C, Yanagiya Y, Uemura K, Miyamoto T, Inagaki M, Shishido T, Sugimachi M, and Sunagawa K. High-cut characteristics of the baroreflex neural arc preserve baroreflex gain against pulsatile pressure. Am J Physiol Heart Circ Physiol 282: H1149–H1156, 2002.
9. Kent BB, Drane JW, Blumenstein B, and Manning JW. A mathematical model to assess changes in the baroreceptor reflex. Cardiology 57: 295–310, 1972.
10. McCloskey DI and Mitchell JH. Reflex cardiovascular and respiratory responses originating in exercising muscle. J Physiol 224: 173–186, 1972.
11. McIlveen SA, Hayes SG, and Kaufman MP. Both central command and exercise pressor reflex reset carotid sinus baroreflex. Am J Physiol Heart Circ Physiol 280: H1454–H1463, 2001.
12. Mense S and Stahnke M. Responses in muscle afferent fibres of slow conduction velocity to contractions and ischaemia in the cat. J Physiol 342: 383–397, 1983.
13. Miki K, Yoshimoto M, and Tanimizu M. Acute shifts of baroreflex control of renal sympathetic nerve activity induced by treadmill exercise in rats. J Physiol 548: 313–322, 2003.
14. Ogoh S, Wasmund WL, Keller DM, O-Yurvati A, Gallagher KM, Mitchell JH, and Raven PB. Role of central command in carotid baroreflex resetting in humans during static exercise. J Physiol 543: 349–364, 2002.
15. Potts JT, Hand GA, Li J, and Mitchell JH. Central interaction between carotid baroreceptors and skeletal muscle receptors inhibits sympathoexcitation. J Appl Physiol 84: 1158–1165, 1998.
16. Potts JT and Li J. Interaction between carotid baroreflex and exercise pressor reflex depends on baroreceptor afferent input. Am J Physiol Heart Circ Physiol 274: H1841–H1847, 1998.
17. Potts JT and Mitchell JH. Rapid resetting of carotid baroreceptor reflex by afferent input from skeletal muscle receptors. Am J Physiol Heart Circ Physiol 275: H2000–H2008, 1998.
18. Potts JT, Paton JF, Mitchell JH, Garry MG, Kline G, Anguelov PT, and Lee SM. Contraction-sensitive skeletal muscle afferents inhibit arterial baroreceptor signalling in the nucleus of the solitary tract: role of intrinsic GABA interneurons. Neuroscience 119: 201–214, 2003.
19. Rowell LB, O'Leary DS, and Kellogg DS. Integration of cardiovascular control system in dynamic exercise. In: Handbook of Physiology. Exercise: Regulation and Integration of Multiple Systems. Bethesda, MD: Am. Physiol. Soc., 1996, sect. 12, chapt. 17, p. 770–838.
20. Sato T, Kawada T, Shishido T, Sugimachi M, Alexander J Jr, and Sunagawa K. Novel therapeutic strategy against central baroreflex failure: a bionic baroreflex system. Circulation 100: 299–304, 1999.
21. Sato T, Kawada T, Sugimachi M, and Sunagawa K. Bionic technology revitalizes native baroreflex function in rats with baroreflex failure. Circulation 106: 730–734, 2002.
22. Smith SA, Querry RG, Fadel PJ, Gallagher KM, Stromstad M, Ide K, Raven PB, and Secher NH. Partial blockade of skeletal muscle somatosensory afferents attenuates baroreflex resetting during exercise in humans. J Physiol 551: 1013–1021, 2003.
23. Stebbins CL, Brown B, Levin D, and Longhurst JC. Reflex effect of skeletal muscle mechanoreceptor stimulation on the cardiovascular system. J Appl Physiol 65: 1539–1547, 1988.
24. Tallarida G, Baldoni F, Peruzzi G, Raimondi G, Massaro M, and Sangiorgi M. Cardiovascular and respiratory reflexes from muscles during dynamic and static exercise. J Appl Physiol 50: 784–791, 1981.
25. Wilson LB, Dyke CK, Pawelczyk JA, Wall PT, and Mitchell JH. Cardiovascular and renal nerve responses to static muscle contraction of decerebrate rabbits. J Appl Physiol 77: 2449–2455, 1994.
26. Yamamoto K, Kawada T, Kamiya A, Takaki H, Miyamoto T, Sugimachi M, and Sunagawa K. Muscle mechanoreflex induces the pressor response by resetting the arterial baroreflex neural arc. Am J Physiol Heart Circ Physiol 286: H1382–H1388, 2004.
27. Yanagiya Y, Sato T, Kawada T, Inagaki M, Tatewaki T, Zheng C, Kamiya A, Takaki H, Sugimachi M, and Sunagawa K. Bionic epidural stimulation restores arterial pressure regulation during orthostasis. J Appl Physiol 97: 984–990, 2004.

This article has been cited by other articles:

				J. M. Stewart, L. D. Montgomery, J. L. Glover, and M. S. Medow Changes in regional blood volume and blood flow during static handgrip Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H215 - H223. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) All Versions of this Article: 289/4/H1604    most recent 00053.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Yamamoto, K. Articles by Sunagawa, K. Search for Related Content PubMed PubMed Citation Articles by Yamamoto, K. Articles by Sunagawa, K.