c-Fos expression in the midbrain periaqueductal gray during static muscle contraction

2000 ◽  
Vol 279 (6) ◽  
pp. H2986-H2993 ◽  
Author(s):  
Jianhua Li ◽  
Jere H. Mitchell
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Neuronal Cells ◽  
Cardiovascular Responses ◽  
Periaqueductal Gray ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Static Contraction ◽  
Afferent Inputs ◽  
Pressor Reflex

The periaqueductal gray (PAG) of the midbrain is involved in the autonomic regulation of the cardiovascular system. The purpose of this study was to determine if static contraction of the skeletal muscle, which increases arterial blood pressure and heart rate, activates neuronal cells in the PAG by examining Fos-like immunoreactivity (FLI). Muscle contraction was induced by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in anesthetized cats. An intravenous infusion of phenylephrine (PE) was used to selectively activate arterial baroreceptors. Extensive FLI was observed within the ventromedial region (VM) of the rostral PAG, the dorsolateral (DL), lateral (L), and ventrolateral (VL) regions of the middle and caudal PAG in barointact animals with muscle contractions, and in barointact animals with PE infusion. However, muscle contraction caused a lesser number of FLI in the VM region of the rostral PAG, the DL, L, and VL regions of the middle PAG and the L and VL regions of the caudal PAG after barodenervation compared with barointact animals. Additionally, the number of FLI in the DL and L regions of the middle PAG was greater in barodenervated animals with muscle contraction than in barodenervated control animals. Thus these results indicated that both muscle receptor and baroreceptor afferent inputs activate neuronal cells in regions of the PAG during muscle contraction. Furthermore, afferents from skeletal muscle activate neurons in specific regions of the PAG independent of arterial baroreceptor input. Therefore, neuronal cells in the PAG may play a role in determining the cardiovascular responses during the exercise pressor reflex.

Exercise pressor reflex function in female rats fluctuates with the estrous cycle

2012 ◽  
Vol 113 (5) ◽  
pp. 719-726 ◽  
Author(s):  
Satoshi Koba ◽  
Kenshi Yoshinaga ◽  
Sayaka Fujita ◽  
Michio Miyoshi ◽  
Tatsuo Watanabe
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Estrous Cycle ◽  
Plasma Concentrations ◽  
Female Rats ◽  
Lumbar Spinal Cord ◽  
Exercise Pressor Reflex ◽  
Skeletal Muscle Contraction ◽  
Static Contraction ◽  
Pressor Reflex

In women, sympathoexcitation during static handgrip exercise is reduced during the follicular phase of the ovarian cycle compared with the menstrual phase. Previous animal studies have demonstrated that estrogen modulates the exercise pressor reflex, a sympathoexcitatory mechanism originating in contracting skeletal muscle. The present study was conducted in female rats to determine whether skeletal muscle contraction-evoked reflex sympathoexcitation fluctuates with the estrous cycle. The estrous cycle was judged by vaginal smear. Plasma concentrations of estrogen were significantly ( P < 0.05) higher in rats during the proestrus phase of the estrus cycle than those during the diestrus phase. In decerebrate rats, either electrically induced 30-s continuous static contraction of the hindlimb muscle or 30-s passive stretch of Achilles tendon (a maneuver that selectively stimulates mechanically sensitive muscle afferents) evoked less renal sympathoexcitatory and pressor responses in the proestrus animals than in the diestrus animals. Renal sympathoexcitatory response to 1-min intermittent (1- to 4-s stimulation to relaxation) bouts of static contraction was also significantly less in the proestrus rats than that in the diestrus rats. In ovariectomized female rats, 17β-estradiol applied into a well covering the dorsal surface of the lumbar spinal cord significantly reduced skeletal muscle contraction-evoked responses. These observations demonstrate that the exercise pressor reflex function and its mechanical component fluctuate with the estrous cycle in rats. Estrogen may cause these fluctuations through its attenuating effects on the spinal component of the reflex arc.

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

1998 ◽  
Vol 274 (5) ◽  
pp. H1841-H1847 ◽  
Author(s):  
Jeffrey T. Potts ◽  
Jianhua Li
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Afferent Input ◽  
Muscle Stretch ◽  
Exercise Pressor Reflex ◽  
Muscle Receptor ◽  
Pressor Reflex ◽  
Passive Muscle

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-S1ventral root stimulation) or passive muscle stretch. Experiments were performed in α-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.

scholarly journals Proteinase-Activated Receptor-2 Sensitivity of Amplified TRPA1 Activity in Skeletal Muscle Afferent Nerves and Exercise Pressor Reflex in Rats with Femoral Artery Occlusion

2017 ◽  
Vol 44 (1) ◽  
pp. 163-171 ◽  
Author(s):  
Jihong Xing ◽  
Jianhua Li
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Contraction ◽  
Femoral Artery ◽  
Transient Receptor Potential ◽  
Drg Neurons ◽  
Artery Ligation ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Pressor Reflex

Background/Aims: Limb ischemia occurs in peripheral artery disease (PAD). Sympathetic nerve activity (SNA) that regulates blood flow directed to the ischemic limb is exaggerated during exercise in this disease, and transient receptor potential channel A1 (TRPA1) in thin-fiber muscle afferents contributes to the amplified sympathetic response. The purpose of the present study was to determine the role of proteinase-activated receptor-2 (PAR2) in regulating abnormal TRPA1 function and the TRPA1-mediated sympathetic component of the exercise pressor reflex. Methods: A rat model of femoral artery ligation was employed to study PAD. Dorsal root ganglion (DRG) tissues were obtained to examine the protein levels of PAR2 using western blot analysis. Current responses induced by activation of TRPA1 in skeletal muscle DRG neurons were characterized using whole-cell patch clamp methods. The blood pressure response to static exercise (i.e., muscle contraction) and stimulation of TRPA1 was also examined after a blockade of PAR2. Results: The expression of PAR2 was amplified in DRG neurons of the occluded limb, and PAR2 activation with SL-NH2 (a PAR2 agonist) increased the amplitude of TRPA1 currents to a greater degree in DRG neurons of the occluded limb. Moreover, FSLLRY-NH2 (a PAR antagonist) injected into the arterial blood supply of the hindlimb muscles significantly attenuated the pressor response to muscle contraction and TRPA1 stimulation in rats with occluded limbs. Conclusions: The PAR2 signal in muscle sensory nerves contributes to the amplified exercise pressor reflex via TRPA1 mechanisms in rats with femoral artery ligation. These findings provide a pathophysiological basis for autonomic responses during exercise activity in PAD, which may potentially aid in the development of therapeutic approaches for improvement of blood flow in this disease.

Estrogen attenuates the cardiovascular and ventilatory responses to central command in cats

2002 ◽  
Vol 92 (4) ◽  
pp. 1635-1641 ◽  
Author(s):  
Shawn G. Hayes ◽  
Nicolas B. Moya Del Pino ◽  
Marc P. Kaufman
Keyword(s):  
Triceps Surae ◽  
Central Command ◽  
Neuronal Function ◽  
Ventilatory Responses ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Static Contraction ◽  
17Β Estradiol ◽  
Pressor Reflex ◽  
Triceps Surae Muscles

Static exercise is well known to increase heart rate, arterial blood pressure, and ventilation. These increases appear to be less in women than in men, a difference that has been attributed to an effect of estrogen on neuronal function. In decerebrate male cats, we examined the effect of estrogen (17β-estradiol; 0.001, 0.01, 0.1, and 1.0 μg/kg iv) on the cardiovascular and ventilatory responses to central command and the exercise pressor reflex, the two neural mechanisms responsible for evoking the autonomic and ventilatory responses to exercise. We found that 17β-estradiol, in each of the three doses tested, attenuated the pressor, cardioaccelerator, and phrenic nerve responses to electrical stimulation of the mesencephalic locomotor region (i.e., central command). In contrast, none of the doses of 17β-estradiol had any effect on the pressor, cardioaccelerator, and ventilatory responses to static contraction or stretch of the triceps surae muscles. We conclude that, in decerebrate male cats, estrogen injected intravenously attenuates cardiovascular and ventilatory responses to central command but has no effect on responses to the exercise pressor reflex.

scholarly journals Exaggerated cardiovascular responses to muscle contraction and tendon stretch in UCD type-2 diabetes mellitus rats

2019 ◽  
Vol 317 (2) ◽  
pp. H479-H486 ◽  
Author(s):  
Ann-Katrin Grotle ◽  
Charles K. Crawford ◽  
Yu Huo ◽  
Kai M. Ybarbo ◽  
Michelle L. Harrison ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cardiovascular Responses ◽  
Exercise Pressor Reflex ◽  
Static Contraction ◽  
Pressor Reflex ◽  
Blood Pressure Responses

Patients with type-2 diabetes mellitus (T2DM) have exaggerated sympathetic activity and blood pressure responses to exercise. However, the underlying mechanisms for these responses, as well as how these responses change throughout disease progression, are not completely understood. For this study, we examined the effect of the progression of T2DM on the exercise pressor reflex, a critical neurocardiovascular mechanism that functions to increase sympathetic activity and blood pressure during exercise. We also aimed to examine the effect of T2DM on reflexive cardiovascular responses to static contraction, as well as those responses to tendon stretch when an exaggerated exercise pressor reflex was present. We evoked the exercise pressor reflex and mechanoreflex by statically contracting the hindlimb muscles and stretching the Achilles tendon, respectively, for 30 s. We then compared pressor and cardioaccelerator responses in unanesthetized, decerebrated University of California Davis (UCD)-T2DM rats at 21 and 31 wk following the onset of T2DM to responses in healthy nondiabetic rats. We found that the pressor response to static contraction was greater in the 31-wk T2DM [change in mean arterial pressure (∆MAP) = 39 ± 5 mmHg] but not in the 21-wk T2DM (∆MAP = 24 ± 5 mmHg) rats compared with nondiabetic rats (∆MAP = 18 ± 2 mmHg; P < 0.05). Similarly, the pressor and the cardioaccelerator responses to tendon stretch were significantly greater in the 31-wk T2DM rats [∆MAP = 69 ± 6 mmHg; change in heart rate (∆HR) = 28 ± 4 beats/min] compared with nondiabetic rats (∆MAP = 14 ± 2 mmHg; ∆HR = 5 ± 3 beats/min; P < 0.05). These findings suggest that the exercise pressor reflex changes as T2DM progresses and that a sensitized mechanoreflex may play a role in exaggerating these cardiovascular responses. NEW & NOTEWORTHY This is the first study to provide evidence that as type-2 diabetes mellitus (T2DM) progresses, the exercise pressor reflex becomes exaggerated, an effect that may be due to a sensitized mechanoreflex. Moreover, these findings provide compelling evidence suggesting that impairments in the reflexive control of circulation contribute to exaggerated blood pressure responses to exercise in T2DM.

Vasopressin acts in the area postrema to attenuate the exercise pressor reflex in anesthetized cats

1998 ◽  
Vol 274 (6) ◽  
pp. H2116-H2122 ◽  
Author(s):  
Charles L. Stebbins ◽  
Stefani Bonigut ◽  
Lea R. Liviakis ◽  
Paul A. Munch
Keyword(s):  
Blood Pressure ◽  
Area Postrema ◽  
Cardiovascular Response ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Baroreflex Function ◽  
Static Contraction ◽  
Before And After ◽  
Pressor Reflex ◽  
Anesthetized Cat

Circulating arginine vasopressin (AVP) can enhance baroreflex function via its action in the area postrema (AP). We tested the hypothesis that AVP acts in the AP to enhance baroreflex function during static contraction and, in turn, attenuates the exercise pressor reflex. Thus mean arterial blood pressure ( n = 9) and heart rate (HR) ( n = 9) during 30 s of electrically stimulated hindlimb contraction were compared before and after bilateral microinjections of 200 nl of the AVP V1-receptor antagonist d(CH2)5Tyr(Me)-AVP (V1x) (1 ng/nl) into the AP of the anesthetized cat. This protocol was repeated in three other cats in which sinoaortic denervation (SAD) was performed before any intervention. Injection of V1xinto the AP had no effect on baseline blood pressure or HR. However, pressor and HR responses to static contraction were augmented by 44 ± 10 and 29 ± 9%, respectively. Static contraction also increased plasma AVP from 15.9 ± 2.0 to 25.5 ± 3.4 pg/ml. In the SAD cats, microinjection of V1x had no effect on contraction-induced increases in blood pressure or HR. These results suggest that baroreflex opposition of the reflex cardiovascular response to static contraction is enhanced by the action of AVP in the AP.

Augmentation of the exercise pressor reflex in prehypertension: roles of the muscle metaboreflex and mechanoreflex

2013 ◽  
Vol 38 (2) ◽  
pp. 209-215 ◽  
Author(s):  
Hyun-Min Choi ◽  
Charles L. Stebbins ◽  
Og-Taeg Lee ◽  
Hosung Nho ◽  
Joon-Hee Lee ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Percentage Increase ◽  
Muscle Metaboreflex ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Static Contraction ◽  
Pressor Reflex

This study investigated the hemodynamic mechanisms underlying the exaggerated blood pressure response to muscle contraction in prehypertensive humans and the potential role of skeletal muscle metabo- and mechanoreceptors in this response. To accomplish this, changes in peak mean arterial blood pressure (ΔMAP), cardiac output, and total peripheral resistance (ΔTPR) were compared between prehypertensive (n = 23) and normotensive (n = 19) male subjects during 2 min of static contraction (at 50% of maximal tension), 2 min of postexercise muscle ischemia (metaboreflex), and 1 min of passive dorsiflexion of the foot (tendon stretch, mechanoreceptor reflex). These variables were assessed before and during the interventions. Percentage increases from baseline in MAP and TPR in response to the exercise pressor reflex were augmented in the prehypertensives, compared with the normotensives (44% ± 5% vs. 33% ± 4% and 34% ± 15% vs. 2% ± 8%, respectively) (p < 0.05). Metaboreflex-induced increases in MAP and TPR were also augmented in the prehypertensives (28% ± 5% vs. 14% ± 4% and 36% ± 12% vs. 14% ± 9%, respectively) (p < 0.05). In response to the mechanoreflex, no differences in the percentage increase in MAP or TPR were seen between groups. The results indicate that the reflex pressor response to static contraction is augmented in prehypertension and suggest that this phenomenon is due, at least in part, to enhanced activation of metaboreceptors.

scholarly journals Blockade of the TP receptor attenuates the exercise pressor reflex in decerebrated rats with chronic femoral artery occlusion

2011 ◽  
Vol 301 (5) ◽  
pp. H2140-H2146 ◽  
Author(s):  
Anna K. Leal ◽  
Jennifer L. McCord ◽  
Hirotsugu Tsuchimochi ◽  
Marc P. Kaufman
Keyword(s):  
Peripheral Artery Disease ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Muscle Afferents ◽  
Peripheral Artery ◽  
Exercise Pressor Reflex ◽  
Tp Receptor ◽  
Static Contraction ◽  
Pressor Reflex ◽  
Artery Disease

Cyclooxygenase metabolites stimulate or sensitize group III and IV muscle afferents, which comprise the sensory arm of the exercise pressor reflex. The thromboxane (TP) receptor binds several of these metabolites, whose concentrations in the muscle interstitium are increased by exercise under freely perfused conditions and even more so under ischemic conditions, which occur in peripheral artery disease. We showed that the exercise pressor reflex is greater in rats with simulated peripheral artery disease than in rats with freely perfused limbs. These findings prompted us to test the hypothesis that the TP receptor contributes to the exaggerated exercise pressor reflex occurring in a rat model of peripheral artery disease. We compared the cardiovascular responses to static contraction and stretch before and after femoral arterial injections of daltroban (80 μg), a TP receptor antagonist. We performed these experiments in decerebrate rats whose femoral arteries were ligated 72 h before the experiment (a model of simulated peripheral artery disease) and in control rats whose hindlimbs were freely perfused. Daltroban reduced the pressor response to static contraction in both freely perfused ( n = 6; before: Δ12 ± 2 mmHg, after: Δ6 ± 2 mmHg, P = 0.024) and 72-h-ligated rats ( n = 10; before: Δ25 ± 3 mmHg, after: Δ7 ± 4 mmHg, P = 0.001). Likewise, daltroban reduced the pressor response to stretch in the freely perfused group ( n = 9; before: Δ30 ± 3 mmHg, after: Δ17 ± 3 mmHg, P < 0.0001) and in the ligated group ( n = 11; before: Δ37 ± 5 mmHg, after: Δ23 ± 3 mmHg, P = 0.016). Intravenous injections of daltroban had no effect on the pressor response to contraction. We conclude that the TP receptor contributes to the pressor responses evoked by contraction and stretch in both freely perfused rats and rats with simulated peripheral artery disease.

Central integration of muscle reflex and arterial baroreflex in midbrain periaqueductal gray: roles of GABA and NO

2004 ◽  
Vol 287 (3) ◽  
pp. H1312-H1318 ◽  
Author(s):  
Jianhua Li
Keyword(s):  
Muscle Contraction ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Periaqueductal Gray ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Reflex Response ◽  
Arterial Baroreflex ◽  
Pressor Reflex ◽  
Change In Mean

It has been suggested that the midbrain periaqueductal gray (PAG) is a neural integrating site for the interaction between the muscle pressor reflex and the arterial baroreceptor reflex. The underlying mechanisms are poorly understood. The purpose of this study was to examine the roles of GABA and nitric oxide (NO) in modulating the PAG integration of both reflexes. To activate muscle afferents, static contraction of the triceps surae muscle was evoked by electrical stimulation of the L7 and S1 ventral roots of 18 anesthetized cats. In the first group of experiments ( n = 6), the pressor response to muscle contraction was attenuated by bilateral microinjection of muscimol (a GABA receptor agonist) into the lateral PAG [change in mean arterial pressure (ΔMAP) = 24 ± 5 vs. 46 ± 8 mmHg in control]. Conversely, the pressor response was significantly augmented by 0.1 mM bicuculline, a GABAA receptor antagonist (ΔMAP = 65 ± 10 mmHg). In addition, the effect of GABAA receptor blockade on the reflex response was significantly blunted after sinoaortic denervation and vagotomy ( n = 4). In the second group of experiments ( n = 8), the pressor response to contraction was significantly attenuated by microinjection of l-arginine into the lateral PAG (ΔMAP = 26 ± 4 mmHg after l-arginine injection vs. 45 ± 7 mmHg in control). The effect of NO attenuation was antagonized by bicuculline and was reduced after denervation. These data demonstrate that GABA and NO within the PAG modulate the pressor response to muscle contraction and that NO attenuation of the muscle pressor reflex is mediated via arterial baroreflex-engaged GABA increase. The results suggest that the PAG plays an important role in modulating cardiovascular responses when muscle afferents are activated.

Spinal angiotensin II influences reflex cardiovascular responses to muscle contraction

1995 ◽  
Vol 269 (4) ◽  
pp. R864-R868 ◽  
Author(s):  
C. L. Stebbins ◽  
S. Bonigut
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Angiotensin Ii ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Ang Ii ◽  
Exercise Pressor Reflex ◽  
Static Contraction ◽  
Pressor Reflex

We tested the hypothesis that inhibition of angiotensin II (ANG II) AT1 receptors in the thoracic spinal cord attenuates the reflex cardiovascular response to electrically induced hindlimb static contraction (exercise pressor reflex). Consequently, in alpha-chloralose-anesthetized cats, contraction-induced increases in mean arterial blood pressure, maximal rate of rise in left ventricular pressure (dP/dt), and heart rate were compared before and after intrathecal injection of the AT1 receptor antagonist losartan (100 or 1,000 micrograms; n = 7). Losartan significantly diminished increases in blood pressure and maximal dP/dt provoked by static contraction by 33 +/- 5 and 31 +/- 6%, respectively. Conversely, these contraction-induced responses were unaffected by similar injection of ANG II into the lumbosacral spinal cord (n = 5). Moreover, intravenous injection of 100 micrograms losartan did not affect the cardiovascular response to contraction. Our data suggest that ANG II has a excitatory effect on the efferent arm of the exercise pressor reflex, which may be due to a facilitatory action on sympathetic nerve activity.

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