| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Division of Cardiovascular Medicine, Departments of Internal Medicine and Human Physiology, University of California, Davis, California 95616
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The
exercise pressor reflex, which arises from the contraction-induced
stimulation of group III and IV muscle afferents, is widely believed to
be evoked by metabolic stimuli signaling a mismatch between
blood/oxygen demand and supply in the working muscles. Nevertheless,
mechanical stimuli may also play a role in evoking the exercise pressor
reflex. To determine this role, we examined the effect of gadolinium,
which blocks mechanosensitive channels, on the exercise pressor reflex
in both decerebrate and 
-chloralose-anesthetized cats. We found that
gadolinium (10 mM; 1 ml) injected into the femoral artery significantly
attenuated the reflex pressor responses to static contraction of the
triceps surae muscles and to stretch of the calcaneal (Achilles)
tendon. In contrast, gadolinium had no effect on the reflex pressor
response to femoral arterial injection of capsaicin (5 µg). In
addition, gadolinium significantly attenuated the responses of group
III muscle afferents, many of which are mechanically sensitive, to both
static contraction and to tendon stretch. Gadolinium, however, had no
effect on the responses of group IV muscle afferents, many of which are
metabolically sensitive, to either static contraction or to capsaicin
injection. We conclude that mechanical stimuli arising in contracting
skeletal muscles contribute to the elicitation of the exercise pressor reflex.
group III and IV muscle afferents; contraction; tendon stretch; capsaicin; autonomic nervous system
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
THE EXERCISE PRESSOR REFLEX (18) has been firmly established to be one of the mechanisms responsible for evoking the autonomic and ventilatory responses to static exercise (5, 11, 19, 34). This reflex arises from the contraction-induced stimulation of thin fiber (i.e., group III and IV) muscle afferents (14). Histologically, the endings of many group III afferents are found in connective tissue, whereas the endings of many group IV afferents are found in the walls of small vessels within the muscle (36). The reflex is widely believed to be evoked by muscle metabolites, such as bradykinin (32), prostaglandins (33), lactic acid (24), phosphate (30), and potassium (27). Moreover, there is substantial electrophysiological evidence demonstrating that these metabolic stimuli increase the discharge rate of group III and IV muscle afferents (2, 11, 13, 17).
Nevertheless, some thin fiber muscle afferents, especially those with group III fibers, have been shown to be responsive to mechanical stimuli that are far below the noxious threshold (1, 12, 17, 22). Moreover, mechanical stimuli, such as tendon stretch, have been shown to evoke impressive autonomic and ventilatory responses (31, 35, 38). Despite these findings, the contribution of thin fiber mechanoreceptors to the exercise pressor reflex is not clear.
Mechanosensitive channels in several types of tissues have been shown to be blocked by gadolinium, a trivalent lanthanide (29, 39). Consequently, gadolinium might serve as a tool to determine the role played by mechanosensitive thin fiber afferents in evoking the exercise pressor reflex. Therefore, we examined the effect of gadolinium injected into the arterial supply of the triceps surae muscles on the autonomic and ventilatory responses of cats to three maneuvers: static contraction, calcaneal (Achilles) tendon stretch, and femoral arterial injection of capsaicin. The first maneuver combined mechanical and metabolic stimuli to evoke reflex increases in arterial pressure, heart rate, and ventilation (i.e., the exercise pressor reflex) (18). The second maneuver used only a mechanical stimulus to evoke reflex increases in arterial pressure, heart rate, and ventilation (31, 38). The third maneuver used only a chemical stimulus to evoke these reflex responses (4). We hypothesized that gadolinium would attenuate the reflex responses to both static contraction and tendon stretch but would have no effect on the reflex response to capsaicin injection.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The cats were anesthetized with a mixture of 5% halothane and oxygen. Catheters were placed in the right jugular vein and common carotid artery for delivery of drugs and measurement of arterial blood pressure, respectively. The carotid artery catheter was connected to a pressure transducer (model P23 XL, Statham) to measure arterial pressure. Heart rate was calculated beat to beat from the arterial pressure pulse by a Gould Biotach amplifier. The trachea was cannulated, and the lungs were ventilated mechanically (Harvard Apparatus) for the remainder of the surgical preparation. For measuring minute ventilation, a pneumotachograph (Fleisch) was attached in-line with the tracheal cannula. PCO2 was maintained between 35 and 40 mmHg by adjusting ventilation. Arterial pH was maintained between 7.35 and 7.45 by adjusting ventilation and by intravenous administration of sodium bicarbonate.
The triceps surae muscles were isolated. The calcaneal bone was severed and attached to a force transducer (model FT-10C, Grass). In experiments in which afferent activity was recorded, the hindlimb was denervated as thoroughly as possible except for the input from the triceps surae muscles.
A catheter was fed through the right femoral artery and external iliac artery to the abdominal aorta. The catheter was secured into place and the caudal artery was tied off, leaving only the left external iliac artery open, where the tip of the catheter was placed. Adjustable ligatures were placed above the catheter on the abdominal aorta and on the common iliac vein to trap the gadolinium in the leg. The cat was then placed in a Kopf stereotaxic head and spinal frame for the remaining procedures.
In all of the cats, a L4-S1 laminectomy was performed to expose the spinal cord. With the use of the skin on the back, a pool was formed and filled with mineral oil to protect the nerves from dessication. The ventral and dorsal roots were identified and separated. In both the reflex and electrophysiological experiments, the L7 and S1 ventral roots were isolated and cut, and the distal segments were placed on stimulating electrodes. The peripheral ends of the dorsal roots were placed on a plastic platform, and the roots were split into thin filaments. Segments of the nerve were split and placed on a bipolar recording electrode until single group III or IV afferent impulse activity was identified (12). The electrophysiological signals were fed into a high-impedance probe (model HIP511, Grass), filtered with a fourth-order low-pass Bessel filter, and then amplified (model P511, Grass) and displayed on a storage oscilloscope (Hewlett-Packard) and monitor (model V1000, Gould).
-Chloralose-Anesthetized and Decerebrate Cats
-chloralose (50 mg/kg iv). Fifteen minutes later, the halothane was
discontinued. Supplemental doses of -chloralose (5-10 mg/kg iv)
were given to maintain anesthesia after the surgical preparation was
completed. The cat was allowed to breathe spontaneously. In the
decerebrate preparation, a midcollicular section was performed under
halothane anesthesia. All of the neural tissue rostral to the section
was removed. Hemostasis was achieved and the cranial vault was filled with agar (37°C). The cat was then removed from the halothane and the
ventilator and allowed to breathe spontaneously.
Gadolinium
Gadolinium (Aldrich) was prepared in buffered HEPES (pH 7.3-7.45, 10 mM concentration, Aldrich) as described by Hajduczok et al. (7). One milliliter of 10 mM gadolinium trichloride was injected into the femoral artery and flushed with 1 ml of normal saline. Both the arterial and venous ligatures were tightened, and the gadolinium was trapped in the leg for 15 min and then released to circulate systematically. As a control, lanthanum trichloride, another trivalent lanthanide, was also trapped in the leg by using the same procedures. As an additional control, 1 ml of 10 mM gadolinium trichloride was injected intravenously (not trapped in the leg), and the reflex experimental protocols were conducted.Experimental Protocol
The pressor reflex. Three stimuli were used to evoke a pressor reflex: tendon stretch, a purely mechanical stimulus; static contraction, a combined mechanical and metabolic stimulus; and capsaicin injection, a purely chemical stimulus. For tendon stretch, the calcaneal tendon was attached to a force transducer. A known tension was applied by using a rack and pinion to the triceps surae muscles for 1 min. Arterial blood pressure, heart rate, and minute ventilation were measured for 60 s before, during, and after tendon stretch. The triceps surae muscles were also statically contracted for 60 s by electrically stimulating the L7 and S1 ventral roots (40 Hz, 0.1 ms, and 1.5-3 times motor threshold). Again, arterial blood pressure, heart rate, and minute ventilation were measured for 1 min before, during, and after static contraction. Finally, 5 µg of capsaicin were injected into the femoral artery, while the same variables were measured. Tendon stretch, static contraction, and capsaicin injection were performed during a control period and at 15 min intervals for up to 3 h after trapping 1 ml of 10 mM gadolinium in the vasculature of the left leg.
Recording single-unit activity from group III and IV muscle afferents. Once the receptive field of a group III or IV afferent was located in the triceps surae muscles, the same experimental protocols were followed as those described above. However, the impulse activity was counted in response to the various stimuli: tendon stretch, static contraction, and capsaicin injection.
Data Analysis
Values for mean arterial blood pressure, heart rate, minute ventilation, and nerve discharge rates are expressed as means ± SE. Baseline values for mean arterial pressure and heart rate were taken immediately before a maneuver; peak values represent the highest level achieved during a maneuver. Ventilation was calculated as a minute volume (i.e., for 60 s) immediately before (i.e., baseline) and during a maneuver (peak). Baseline afferent discharge was counted over the 60-s period immediately before a maneuver, and peak discharge was counted for the entire 60 s of tendon stretch and static contraction. For capsaicin injection, peak discharge was counted for the duration of the response, which was composed of a burst lasting 5-8 s. All of the discharge rates were converted into impulses per second. Statistical analyses were conducted by using SigmaStat version 2.0 software, and all of the tests were two-way repeated measures ANOVA unless otherwise stated. When appropriate, Tukey's post hoc tests were used. The criteria for statistical significance was P < 0.05.| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Reflex Experiments
-Chloralose-anesthetized cats.
In -chloralose-anesthetized cats (n = 10),
gadolinium significantly attenuated the pressor responses to static
contraction and to tendon stretch, an effect that reached its peak by
60 min and that recovered by 120 min (Fig.
1). Although baseline heart rate drifted
upward, gadolinium significantly attenuated the cardioaccelerator responses to both tendon stretch and static contraction (Fig. 1). Peak
tensions developed by the triceps surae muscles during static
contraction and tendon stretch are shown in Table
1. In contrast, the pressor,
cardioaccelerator, and ventilatory responses to injection of 5 µg of
capsaicin were not changed (P > 0.05) by gadolinium,
averaging 44 ± 5 mmHg, 19 ± 4 beats/min, and 623 ± 69 ml/min before gadolinium injection and 43 ± 5 mmHg, 22 ± 4 beats/min, and 578 ± 69 ml/min 60 min afterwards. Changes in ventilation during tendon stretch and static contraction were small,
variable, and not influenced by gadolinium injection, findings that led
us to perform further reflex experiments on decerebrate cats (see
below).
|
|
-chloralose-anesthetized cats. In the first experiment, we injected
1 ml of 10 mM lanthanum trichloride into the femoral artery. Like
gadolinium, this latter substance was trapped in leg for 15 min.
Lanthanum, a trivalent cation that is similar in size to gadolinium,
had no effect on the pressor, cardioaccelerator, or ventilatory
responses to static contraction, tendon stretch, or 5 µg capsaicin
injection (n = 5; Fig.
2). In the second experiment, 1 ml of 10 mM gadolinium was injected intravenously, and the reflex protocols were
repeated. Intravenous injection of gadolinium in three
-chloralose-anesthetized cats did not attenuate the pressor,
cardioaccelerator, or ventilatory responses to static
contraction, tendon stretch, or capsaicin injection (Fig.
3).
|
|
Dose response.
In -chloralose-anesthetized cats, we injected into the femoral
artery four different concentrations of gadolinium. The volume was
always 1 ml and the injectate was trapped as described above. Gadolinium in a concentration of 1 mM was ineffective at attenuating the pressor, cardioaccelerator, and ventilatory responses to both static contraction and tendon stretch in -chloralose-anesthetized cats (n = 3). Likewise, gadolinium (5 mM) attenuated
modestly pressor responses to contraction and to tendon stretch
(n = 4). On the other hand, gadolinium (10 mM) was
highly effective in attenuating the reflex responses (see above).
Higher concentrations (25 mM) caused attenuation of the responses but
no recovery within 3 h (n = 3).
Decerebrate Unanesthetized Cats
Mean arterial pressure.
In seven decerebrate cats, gadolinium significantly attenuated
(P < 0.05) the pressor responses to static contraction
and to stretch of the calcaneal tendon, effects that reached their peak
60 min after injection and that recovered 120 min after injection (Fig.
4). Peak tensions developed by the
triceps surae muscles during contraction and stretch are shown in Table
1. At the peak of the effect of gadolinium on the pressor responses to
either contraction or tendon stretch, the pressor response to capsaicin injection (5 µg) was not attenuated. For example, the pressor response to capsaicin before injection of gadolinium averaged 48 ± 5 mmHg; likewise, the pressor response 60 min after injection averaged 50 ± 5 mmHg. Gadolinium did not significantly effect baseline blood pressures (Fig. 4).
|
Heart rate. Heart rate increased significantly (P < 0.05) in response to both static contraction and tendon stretch in decerebrate cats. Gadolinium significantly (P < 0.05) attenuated the cardioaccelerator response to both stimuli (Fig. 4), effects that reached their peaks 60 min after injection and that recovered 120 min after injection. Baseline heart rate increased significantly over time (Fig. 4), a finding that was reported (16) in decerebrate cats that had undergone laminectomies. Gadolinium had no effect on the cardioaccelerator response to capsaicin injection (5 µg). Before gadolinium, the response to capsaicin averaged 33 ± 9 beats/min, and 60 min later, the response averaged 36 ± 9 beats/min.
Ventilation. Minute ventilation significantly increased in response to both static contraction and tendon stretch. Nevertheless, the ventilatory response to contraction was larger than that to stretch. Gadolinium attenuated these responses, effects that reached their peaks 60 min after injection and that recovered 120 min after injection (Fig. 4). Gadolinium had no effect on the ventilatory response to capsaicin, averaging 1,284 ± 101 ml/min before and 1,401 ± 101 ml/min 60 min afterward.
Time course.
In the decerebrate cats, we examined the time course of the pressor,
cardioaccelerator, and ventilatory responses to both static contraction
and tendon stretch before as well as 60 min after femoral arterial
injection of gadolinium (10 mM; n = 7). We found that
gadolinium abolished the pressor and cardioaccelerator responses to
both maneuvers 2 s after their initiation (see Fig. 5). Likewise,
gadolinium markedly decreased these responses 5 s after initiation
(P < 0.05). Gadolinium also reduced the ventilatory responses to both maneuvers at 5 s after their initiation
(P < 0.05).
|
Group III and IV Muscle Afferents
We recorded the discharge of eleven group III and seven group IV afferents, each of which had a receptive field in the triceps surae muscles. Conduction velocities for the group III afferents ranged from 2.7 to 26.0 m/s (13.1 ± 2.7) and for the group IV afferents from 0.8 to 1.8 m/s (1.1 ± 0.1). For four group III afferents and for two group IV afferents, we calculated the conduction velocities before and ~60 min after giving gadolinium. The velocities were unchanged.Responses of group III muscle afferents to static
contraction.
Of the 11 group III afferents, 10 increased their discharge in response
to static contraction of the triceps surae muscles. The discharge rates
of each of the 10 afferents were significantly attenuated
(P < 0.05) by gadolinium during static contraction (Fig. 6). Before gadolinium was given,
static contraction increased afferent discharge rates from 0.1 ± 0.2 to 0.7 ± 0.2 impulse/s (P < 0.05). Sixty
minutes after gadolinium administration, the discharge rate did not
increase in response to static contraction (from 0.2 ± 0.2 to
0.2 ± 0.2 impulse/s). After 120 min, however, the response to
contraction returned to its control levels. Specifically, the discharge
rate for group III afferents increased from 0.3 ± 0.2 to 1.1 ± 0.2 impulse/s in response to static contraction (P < 0.05).
|
Responses to group III muscle afferents to tendon stretch. Of the 11 group III afferents tested, 7 increased their discharge in response to stretch of the calcaneal tendon. The response to stretch of these seven afferents was significantly attenuated by gadolinium (P < 0.05). Before gadolinium was administered, tendon stretch increased afferent discharge from 0.2 ± 0.3 to 1.1 ± 0.3 impulse/s. Sixty minutes after gadolinium administration, tendon stretch increased discharge from 0.2 ± 0.3 to 0.4 ± 0.3 impulse/s. However, at 120 min after gadolinium, the response to tendon stretch returned to control levels. Specifically, tendon stretch increased afferent discharge rates from 0.5 ± 0.3 to 1.1 ± 0.3 impulse/s.
Responses of group III muscle afferents to capsaicin injection. Only two of the eleven group III muscle afferents were stimulated by injection of 5 µg of capsaicin. Whereas the responses of these two afferents to static contraction and tendon stretch were attenuated by gadolinium, the responses of the afferents to capsaicin were unaffected.
Responses of group IV muscle afferents to static
contraction.
Six of the seven group IV muscle afferents responded to static
contraction of the triceps surae muscles. The one afferent that did not
respond to static contraction did respond to capsaicin injection and to
noxious pinching of the muscle. The responses of the six group IV
afferents to static contraction were not significantly affected by
gadolinium injection (Fig. 7).
Specifically, before gadolinium, the discharge increased from 0.07 ± 0.04 to 0.3 ± 0.1 impulse/s. Sixty minutes later, the
discharge increased from 0.09 ± 0.05 to 0.3 ± 0.1 impulse/s.
|
Responses of group IV muscle afferents to tendon stretch. None of the seven group IV muscle afferents responded to tendon stretch, and, therefore, the effect of gadolinium on their responses to this maneuver was not tested.
Responses of group IV muscle afferents to capsaicin injection. Six of the seven group IV muscle afferents responded to injection of 5 µg of capsaicin. Of the six, we were able to quantify the response in four afferents. The remaining two responded so vigorously that we were unable to count the impulses. Qualitatively, these two afferents responded more vigorously as the experiments progressed and did not appear to be attenuated by gadolinium. Quantitatively, the responses to capsaicin of the four group IV afferents were not significantly attenuated by gadolinium. Injection of capsaicin before gadolinium elicited a burst of 14.8 ± 6.1 impulse/s (n = 4). Sixty minutes after gadolinium, the same dose of capsaicin injected caused the afferents to fire 19.8 ± 8.7 impulse/s.
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
We have found that gadolinium, when injected into the femoral
artery of decerebrate unanesthetized cats, attenuated the reflex autonomic and ventilatory responses to both static contraction and to
tendon stretch but had no effect on the responses to capsaicin injection. We also found that gadolinium, injected into the femoral artery of -chloralose-anesthetized cats, attenuated the pressor responses to static contraction and to tendon stretch but had a weak or
no effect on the cardioaccelerator or ventilatory responses to these
stimuli. The lack of robust attenuating effect of gadolinium on the
cardiac and ventilatory responses to static contraction and to tendon
stretch in -chloralose-anesthetized cats was probably due to two
factors. First, the cardioaccelerator responses to these stimuli
are smaller in -chloralose-anesthetized cats than in
decerebrate, unanesthetized cats (10). Consequently, there is less of a response to be attenuated by gadolinium. Second, tendon
stretch in -chloralose-anesthetized cats has been shown to be a weak
and inconsistent ventilatory stimulus, failing to produce hypocapnia
(38).
Gadolinium attenuated the responses of group III afferents to both tendon stretch, a purely mechanical stimulus, as well as to static contraction, a mixed mechanical and metabolic stimulus. In contrast, gadolinium had no effect on the responses of group IV afferents to contraction. These findings are clearly consistent with our hypothesis that gadolinium blocks mechanosensitive channels as well as with what is known about the discharge properties of thin fiber muscle afferents. Specifically, group III afferents respond vigorously to tendon stretch, whereas group IV afferents do not (12). Likewise, group III afferents often respond to static contraction with an explosive burst of impulses at its onset, whereas group IV afferents may discharge an impulse or two at the onset of contraction but discharge most of their impulses 5-30 s later (12, 23). Finally, gadolinium had no effect on the responses of the group III and IV afferents to capsaicin injection, a finding that is consistent with this lanthanide being a specific blocker of mechanosensitive channels.
The mechanism of action of gadolinium on mechanoreception is not well understood. Most likely, this trivalent ion has multiple mechanisms and sites of action depending on its concentration (8). For example, gadolinium has been shown to block nonselectively mechanogated cation channels, L- and T-type calcium channels, and mechanogated potassium channels (8). To understand in part the mechanism of action of gadolinium in our experiments, one must know the concentration of this cation at the receptor, information that is obviously not available.
The use of gadolinium to block the discharge of mechanoreceptors in other reflex systems in mammals has proven to be controversial. Specifically, gadolinium has been shown to attenuate baroreceptor discharge in both rabbits (7) and cats (40) but not in rats (3). We can offer no explanation for these disparate results. Nevertheless, our findings with another type of mechanosensitive afferent, namely the group III muscle afferent, is consistent with the findings of Hajduczok et al. (7) and Zanzinger et al. (40) and suggests that gadolinium might serve as a pharmacological tool with which to study mechanoreceptor contributions to reflex responses.
The exercise pressor reflex is often perceived as a neural mechanism that seeks to correct a mismatch between blood supply and demand in exercising muscles. Specifically, this reflex is thought to be evoked by a muscle metabolite produced by this mismatch (25, 26). Indeed, there is impressive evidence showing that the elicitation of the "muscle metaboreflex" partially restores arterial blood flow to exercising hindlimb muscles (21, 28).
The exercise pressor reflex, in addition to being evoked by a metabolic or chemical stimulus, might also be evoked by a mechanical stimulus. For example, in cats, static contraction of the triceps surae muscles reflexly increased renal sympathetic nerve activity and decreased vagal tone to the heart with a latency of <1 s (15, 35). Moreover, rhythmic intermittent static contraction of these muscles caused the renal nerve to discharge in a synchronous manner (35). Likewise, electrical stimulation of the tibial nerve, which innervates the triceps surae muscles, did not activate the renal nerve until the current intensity reached five times motor threshold, a level that excluded group I and II muscle afferents (35) from comprising the sensory arm of the reflex arc causing the effect. In the present study, we found that gadolinium abolished the short latency (i.e., 2 s) reflex pressor, cardioaccelerator, and ventilatory responses to static contraction. Considered together, these findings led to the conclusion that group III mechanoreceptors, when activated by contraction, are capable of stimulating by a reflex mechanism the sympathetic nervous system in cats.
There is also evidence in humans that mechanoreceptors contribute to reflexes that activate the cardiovascular system. Specifically, passive cycling of the legs, a maneuver that stretches muscles in the absence of contraction, rapidly increased (i.e., within 1 s) heart rate (20). Likewise, compression of the legs, also in the absence of contraction, increased heart rate and arterial pressure (6, 37). Finally, electrically induced static contraction, a maneuver that bypassed central command, has been shown to increase heart rate with a latency of about one-half a second (9).
In conclusion, our study is the first to show that removal of mechanoreceptor output from statically contracting muscles attenuated the exercise pressor reflex. Mechanoreceptor (i.e., group III) responses to static contraction and tendon stretch were prevented by injecting and trapping gadolinium in the vasculature of the hindlimb. In contrast, metaboreceptor (i.e., group IV) responses to contraction as well as to capsaicin were not affected by gadolinium. These findings lead us to speculate that gadolinium exerted its effect on mechanoreceptors in our experiments by blocking stretch-activated ion channels.
| |
ACKNOWLEDGEMENTS |
|---|
We thank Nicolas Moya del Pino and Winnie Pak for technical assistance and Eileen English for typing the manuscript.
| |
FOOTNOTES |
|---|
This work was supported by National Heart, Lung, and Blood Institute Grant HL-30710.
Address for reprint requests and other correspondence: S. G. Hayes, Division of Cardiovascular Medicine, TB 172, 1 Shields Ave., Davis, CA 95616 (E-mail: sghayes{at}ucdavis.edu).
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.
Received 30 August 2000; accepted in final form 14 December 2000.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Adreani, CM,
Hill JM,
and
Kaufman MP.
Responses of group III and IV muscle afferents to dynamic exercise.
J Appl Physiol
86:
1811-1817,
1997.
2.
Adreani, CM,
and
Kaufman MP.
Effect of arterial occlusion on responses of group III and IV afferents to dynamic exercise.
J Appl Physiol
84:
1827-1833,
1998
3.
Andresen, M,
and
Yang M.
Gadolinium and mechanotransduction of rat aortic baroreceptors.
Am J Physiol Heart Circ Physiol
262:
H1415-H1421,
1992
4.
Crayton, SC,
Mitchell JH,
and
Payne FC, III.
Reflex cardiovascular response during the injection of capsaicin into skeletal muscle.
Am J Physiol Heart Circ Physiol
240:
H315-H319,
1981.
5.
Freund, PR,
Rowell LB,
Murphy TM,
Hobbs SF,
and
Butler SH.
Blockade of pressor response to muscle ischemia by sensory nerve block in man.
Am J Physiol Heart Circ Physiol
236:
H433-H439,
1979.
6.
Gaffney, FA,
Thal ER,
Taylor WF,
Bastian BC,
Weigelt JA,
Atkins JM,
and
Blomqvist GG.
Hemodynamic effects of medical anti-shock trousers (MAST garment).
J Trauma
21:
931-937,
1981[Web of Science][Medline].
7.
Hajduczok, G,
Chapleau M,
Ferlic R,
Mao H,
and
Abboud FM.
Gadolinium inhibits mechanoelectrical transduction in rabbit carotid baroreceptors.
J Clin Invest
94:
2392-2396,
1994.
8.
Hamill, OP,
and
McBride DW, Jr.
The pharmacology of mechanogated membrane ion channels (Review).
Pharmacol Rev
48:
231-252,
1996[Abstract].
9.
Hollander, AP,
and
Bouman LN.
Cardiac acceleration in man elicited by a muscle-heart reflex.
J Appl Physiol
38:
272-278,
1975
10.
Iwamoto, GA,
Waldrop TG,
Kaufman MP,
Botterman BR,
Rybicki KJ,
and
Mitchell JH.
Pressor reflex evoked by muscular contraction: contributions by neuraxis levels.
J Appl Physiol
59:
459-467,
1985
11.
Kaufman, MP,
and
Forster HV.
Reflexes controlling circulatory, ventilatory and airway responses to exercise.
In: Handbook of Physiology. Exercise: Regulation and Integration of Multiple Systems. Bethesda, MD: Am. Physiol. Soc, 1996, sect. 12, chapt. 10, p. 381-447.
12.
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
13.
Kaufman, MP,
Rybicki KJ,
Waldrop TG,
and
Ordway GA.
Effect of ischemia on responses of group III and IV afferents to contraction.
J Appl Physiol
57:
644-650,
1984
14.
McCloskey, DI,
and
Mitchell JH.
Reflex cardiovascular and respiratory responses originating in exercising muscle.
J Physiol (Lond)
224:
173-186,
1972
15.
McMahon, SE,
and
McWilliam PN.
Changes in R-R interval at the start of muscle contraction in the decerebrate cat.
J Physiol (Lond)
447:
549-562,
1992
16.
McWilliam, PN,
and
Yang T.
Inhibition of cardiac vagal component of baroreflex by group III and IV afferents.
Am J Physiol Heart Circ Physiol
260:
H730-H734,
1991
17.
Mense, S,
and
Stahnke M.
Responses in muscle afferent fibers of slow conduction velocity to contractions and ischemia in the cat.
J Physiol (Lond)
342:
383-397,
1983
18.
Mitchell, JH,
Kaufman MP,
and
Iwamoto GA.
The exercise pressor reflex: its cardiovascular effects, afferent mechanisms, and central pathways.
Annu Rev Physiol
45:
229-242,
1983[Web of Science][Medline].
19.
Mitchell, JH,
Reeves DR,
Rogers HB,
and
Secher NH.
Epidural anesthesia and cardiovascular responses to static exercise in man.
J Physiol (Lond)
417:
13-24,
1989
20.
Nòbrega, ACL,
and
Araùjo CGS
Heart rate transient at the onset of active and passive dynamic exercise.
Med Sci Sports Exerc
25:
37-41,
1993[Web of Science][Medline].
21.
O'Leary, DS.
Autonomic mechanisms of muscle metaboreflex control of heart rate.
J Appl Physiol
74:
1748-1754,
1993
22.
Pickar, JG,
Hill JM,
and
Kaufman MP.
Dynamic exercise stimulates group III muscle afferents.
J Neurophysiol
71:
753-760,
1994
23.
Rotto, DM,
and
Kaufman MP.
Effects of metabolic products of muscular contraction on the discharge of group III and IV afferents.
J Appl Physiol
64:
2306-2313,
1988
24.
Rotto, DM,
Stebbins CL,
and
Kaufman MP.
Reflex cardiovascular and ventilatory responses to increasing H+ activity in cat hindlimb muscle.
J Appl Physiol
67:
256-263,
1989
25.
Rowell, L,
and
O'Leary D.
Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes.
J Appl Physiol
69:
407-418,
1990
26.
Rowell, LB,
and
Sheriff DD.
Are muscle "chemoreflexes" functionally important?
New Physiol Sci
3:
240-253,
1988.
27.
Rybicki, KJ,
Kaufman MP,
Kenyon JL,
and
Mitchell JH.
Arterial pressure responses to increasing interstitial potassium in hindlimb muscle of dogs.
Am J Physiol Regulatory Integrative Comp Physiol
247:
R717-R721,
1984
28.
Sheriff, DD,
Wyss CR,
Rowell LB,
and
Scher AM.
Does inadequate oxygen delivery trigger pressor response to muscle hypoperfusion during exercise?
Am J Physiol Heart Circ Physiol
253:
H1199-H1207,
1987
29.
Sigurdson, W,
Ruknudin A,
and
Sachs F.
Calcium imaging of mechanically induced fluxed in tissue-cultured chick heart: role of stretch-activated ion channels.
Am J Physiol Heart Circ Physiol
262:
H1110-H1115,
1992
30.
Sinoway, LI,
Smith MB,
Enders B,
Leuenberger U,
Dzwonczyk T,
Gray K,
Whisier S,
and
Moore RL.
Role of diprotonated phosphate in evoking muscle reflex responses in cats and humans.
Am J Physiol Heart Circ Physiol
267:
H770-H778,
1994
31.
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
32.
Stebbins, CL,
and
Longhurst JC.
Bradykinin in reflex cardiovascular response to static muscular contraction.
J Appl Physiol
61:
271-279,
1986
33.
Stebbins, CL,
Maruoka Y,
and
Longhurst JC.
Prostaglandins contribute to cardiovascular reflexes evoked by static muscular contraction.
J Appl Physiol
65:
1539-1547,
1988.
34.
Victor, RG,
Pryor SL,
Secher NH,
and
Mitchell JH.
Effects of partial neuromuscular blockade on sympathetic nerve responses to static exercise in humans.
Circ Res
65:
468-476,
1989
35.
Victor, RG,
Rotto DM,
Pryor SL,
and
Kaufman MP.
Stimulation of renal sympathetic activity by static contraction: evidence for mechanoreceptor-induced reflexes from skeletal muscle.
Circ Res
64:
592-599,
1989
36.
Von During, M,
and
Andres KH.
Topography and ultrastructure of group III and IV nerve terminals of cat's gastrocnemius-soleus muscle.
In: The Primary Afferent Neuron: A Survey of Recent Morpho-Functional Aspects, edited by Zenker W,
and Neuhuber WL.. New York: Plenum, 1990, p. 35-41.
37.
Williamson, JW,
Mitchell JH,
Olesen HL,
Raven PB,
and
Secher NH.
Reflex increase in blood pressure induced by leg compression in man.
J Physiol (Lond)
475:
351-357,
1994
38.
Wilson, LB,
Wall PT,
Pawelczyk JA,
and
Matsukawa K.
Cardiorespiratory and phrenic nerve responses to graded muscle stretch in anesthetized cats.
Respir Physiol
98:
251-266,
1994[Web of Science][Medline].
39.
Yang, XC,
and
Sachs F.
Block of stretch-activated ion channels in Xenopus oocytes by gadolinium and calcium ions.
Science
243:
1068-1071,
1989
40.
Zanziger, J,
Czachurski J,
and
Seller H.
Lack of nitric oxide sensitivity of carotid sinus baroreceptors activated by normal blood pressure stimuli in cats.
Neurosci Lett
208:
121-124,
1996[Web of Science][Medline].
This article has been cited by other articles:
|
|
 |
|
  H. Tsuchimochi, S. G. Hayes, J. L. McCord, and M. P. Kaufman Both central command and exercise pressor reflex activate cardiac sympathetic nerve activity in decerebrate cats Am J Physiol Heart Circ Physiol, April 1, 2009; 296(4): H1157 - H1163. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. G. Hayes, J. L. McCord, S. Koba, and M. P. Kaufman Gadolinium inhibits group III but not group IV muscle afferent responses to dynamic exercise J. Physiol., February 15, 2009; 587(4): 873 - 882. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. G. Hayes, J. L. McCord, J. Rainier, Z. Liu, and M. P. Kaufman Role played by acid-sensitive ion channels in evoking the exercise pressor reflex Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1720 - H1725. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Yamamoto, T. Kawada, A. Kamiya, H. Takaki, T. Shishido, K. Sunagawa, and M. Sugimachi Muscle mechanoreflex augments arterial baroreflex-mediated dynamic sympathetic response to carotid sinus pressure Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H1081 - H1089. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Cui, R. Moradkhan, V. Mascarenhas, A. Momen, and L. I. Sinoway Cyclooxygenase inhibition attenuates sympathetic responses to muscle stretch in humans Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2693 - H2700. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Cui, V. Mascarenhas, R. Moradkhan, C. Blaha, and L. I. Sinoway Effects of muscle metabolites on responses of muscle sympathetic nerve activity to mechanoreceptor(s) stimulation in healthy humans Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2008; 294(2): R458 - R466. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Williams, S. A. Smith, D. E. O'Brien, J. H. Mitchell, and M. G. Garry The group IV afferent neuron expresses multiple receptor alterations in cardiomyopathyic rats: evidence at the cannabinoid CB1 receptor J. Physiol., February 1, 2008; 586(3): 835 - 845. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Matsukawa and T. Nakamoto Muscle mechanosensitive reflex is suppressed in the conscious condition: effect of anesthesia J Appl Physiol, January 1, 2008; 104(1): 82 - 87. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. E. Kindig, S. G. Hayes, and M. P. Kaufman Blockade of purinergic 2 receptors attenuates the mechanoreceptor component of the exercise pressor reflex Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H2995 - H3000. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Nakamoto and K. Matsukawa Muscle mechanosensitive receptors close to the myotendinous junction of the Achilles tendon elicit a pressor reflex J Appl Physiol, June 1, 2007; 102(6): 2112 - 2120. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Matsukawa, T. Nakamoto, and A. Inomoto Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H121 - H129. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. P. Kaufman Mechanoreceptors and central command Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H117 - H118. [Full Text] [PDF]
|
|
|
|
|
|
J. Cui, C. Blaha, R. Moradkhan, K. S. Gray, and L. I. Sinoway Muscle sympathetic nerve activity responses to dynamic passive muscle stretch in humans J. Physiol., October 15, 2006; 576(2): 625 - 634. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. G. Hayes, A. E. Kindig, and M. P. Kaufman Cyclooxygenase blockade attenuates responses of group III and IV muscle afferents to dynamic exercise in cats Am J Physiol Heart Circ Physiol, June 1, 2006; 290(6): H2239 - H2246. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. E. Kindig, S. G. Hayes, R. L. Hanna, and M. P. Kaufman P2 antagonist PPADS attenuates responses of thin fiber afferents to static contraction and tendon stretch Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1214 - H1219. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. G. Hayes, A. E. Kindig, and M. P. Kaufman Comparison between the effect of static contraction and tendon stretch on the discharge of group III and IV muscle afferents J Appl Physiol, November 1, 2005; 99(5): 1891 - 1896. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Yamamoto, T. Kawada, A. Kamiya, H. Takaki, T. Miyamoto, M. Sugimachi, and K. Sunagawa Muscle mechanoreflex induces the pressor response by resetting the arterial baroreflex neural arc Am J Physiol Heart Circ Physiol, April 1, 2004; 286(4): H1382 - H1388. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Hayashi Exercise pressor reflex in decerebrate and anesthetized rats Am J Physiol Heart Circ Physiol, June 1, 2003; 284(6): H2026 - H2033. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
E) was significantly greater
(P < 0.05) than the corresponding baseline value
(means ± SE are given inside bars).
) and 60 min after
(
) gadolinium injection into the femoral artery
(n = 7). Circles represent means, and brackets
represent ±SE. Circles at time 0 represent baseline
(i.e., before the maneuver). First circle after time 0 represents the mean 2 s after the maneuver started, and every
circle afterwards represents the mean at 5-s intervals starting from
time 0. Time period when the muscles were contracted or
stretched is represented by the filled horizontal bar. During
contraction and stretch, all means for 
MAP and 
