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.

Reflex cardiovascular responses evoked by selective activation of skeletal muscle ergoreceptors

2001 ◽  
Vol 90 (1) ◽  
pp. 308-316 ◽  
Author(s):  
B. G. Leshnower ◽  
J. T. Potts ◽  
M. G. Garry ◽  
J. H. Mitchell
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Cardiovascular Response ◽  
Afferent Fiber ◽  
Cardiovascular Responses ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Muscle Stretch ◽  
Group Iii ◽  
Passive Muscle

It is well known that the exercise pressor reflex (EPR) is mediated by group III and IV skeletal muscle afferent fibers, which exhibit unique discharge responses to mechanical and chemical stimuli. Based on the difference in discharge patterns of group III and IV muscle afferents, we hypothesized that activation of mechanically sensitive (MS) fibers would evoke a different pattern of cardiovascular responses compared with activation of both MS and chemosensitive (CS) fibers. Experiments were conducted in chloralose-urethane-anesthetized cats ( n = 10). Passive muscle stretch was used to activate MS afferents, and electrically evoked contraction of the triceps surae was used to activate both MS and CS muscle afferents. No significant differences were shown in reflex heart rate and mean arterial pressure (MAP) responses between passive muscle stretch and evoked muscle contraction. However, when the reflex responses were matched according to tension-time index (TTI), the peak MAP response (67 ± 4 vs. 56 ± 4 mmHg, P < 0.05) was significantly greater at higher TTI (427 ± 18 vs. 304 ± 13 kg · s, high vs. low TTI, P < 0.05), despite different modes of afferent fiber activation. When the same mode of afferent fiber activation was compared, the peak MAP response (65 ± 7 vs. 55 ± 5 mmHg, P < 0.05) was again predicted by the magnitude of TTI (422 ± 24 vs. 298 ± 19 kg · s, high vs. low TTI, P < 0.05). Total sensory input from skeletal muscle ergoreceptors, as predicted by TTI and not the modality of afferent fiber activation (muscle contraction vs. passive stretch), is suggested to be the primary determinant of the magnitude of the EPR-evoked cardiovascular response.

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.

scholarly journals Dynamic exercise training prevents exercise pressor reflex overactivity in spontaneously hypertensive rats

2015 ◽  
Vol 309 (5) ◽  
pp. H762-H770 ◽  
Author(s):  
Masaki Mizuno ◽  
Gary A. Iwamoto ◽  
Wanpen Vongpatanasin ◽  
Jere H. Mitchell ◽  
Scott A. Smith
Keyword(s):  
Exercise Training ◽  
Muscle Contraction ◽  
Spontaneously Hypertensive Rats ◽  
Wheel Running ◽  
Cardiovascular Responses ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Renal Sympathetic

Cardiovascular responses to exercise are exaggerated in hypertension. We previously demonstrated that this heightened cardiovascular response to exercise is mediated by an abnormal skeletal muscle exercise pressor reflex (EPR) with important contributions from its mechanically and chemically sensitive components. Exercise training attenuates exercise pressor reflex function in healthy subjects as well as in heart failure rats. However, whether exercise training has similar physiological benefits in hypertension remains to be elucidated. Thus we tested the hypothesis that the EPR overactivity manifest in hypertension is mitigated by exercise training. Changes in mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) in response to muscle contraction, passive muscle stretch, and hindlimb intra-arterial capsaicin administration were examined in untrained normotensive Wistar-Kyoto rats (WKYUT; n = 6), exercise-trained WKY (WKYET; n = 7), untrained spontaneously hypertensive rats (SHRUT; n = 8), and exercise-trained SHR (SHRET; n = 7). Baseline MAP after decerebration was significantly decreased by 3 mo of wheel running in SHRET (104 ± 9 mmHg) compared with SHRUT (125 ± 10 mmHg). As previously reported, the pressor and renal sympathetic responses to muscle contraction, stretch, and capsaicin administration were significantly higher in SHRUT than WKYUT. Exercise training significantly attenuated the enhanced contraction-induced elevations in MAP (SHRUT: 53 ± 11 mmHg; SHRET: 19 ± 3 mmHg) and RSNA (SHRUT: 145 ± 32%; SHRET: 57 ± 11%). Training produced similar attenuating effects in SHR during passive stretch and capsaicin administration. These data demonstrate that the abnormally exaggerated EPR function that develops in hypertensive rats is significantly diminished by exercise training.

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.

Effects of type 1 diabetes on reflexive cardiovascular responses to intermittent muscle contraction

2020 ◽  
Vol 319 (3) ◽  
pp. R358-R365
Author(s):  
Ann-Katrin Grotle ◽  
Yu Huo ◽  
Michelle L. Harrison ◽  
Junghoon Lee ◽  
Kai M. Ybarbo ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Muscle Contraction ◽  
Type 1 Diabetes Mellitus ◽  
Early Stage ◽  
Cardiovascular Responses ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Cardiovascular Strain

This is the first study to provide evidence that early-stage type 1 diabetes mellitus (T1DM) leads to an exaggerated exercise pressor reflex evoked by intermittent muscle contraction, resulting in substantially higher cardiovascular strain. These findings are significant as they indicate that interventions targeting the exercise pressor reflex may work to alleviate the increased cardiovascular strain and overall burden during exercise in T1DM.

scholarly journals Bradykinin B2 receptor contributes to the exaggerated muscle mechanoreflex in rats with femoral artery occlusion

2013 ◽  
Vol 304 (8) ◽  
pp. H1166-H1174 ◽  
Author(s):  
Jian Lu ◽  
Jihong Xing ◽  
Jianhua Li
Keyword(s):  
Muscle Contraction ◽  
Femoral Artery ◽  
Artery Occlusion ◽  
Receptor Expression ◽  
Muscle Stretch ◽  
Exercise Pressor Reflex ◽  
Femoral Artery Occlusion ◽  
Muscle Mechanoreflex ◽  
Pressor Reflex ◽  
Hoe 140

Static muscle contraction activates the exercise pressor reflex, which in turn increases sympathetic nerve activity (SNA) and blood pressure (BP). Bradykinin (BK) is considered as a muscle metabolite responsible for modulation of the sympathetic and cardiovascular responses to muscle contraction. Prior studies have suggested that kinin B2 receptor mediates the effects of BK on the reflex SNA and BP responses during stimulation of skeletal muscle afferents. In patients with peripheral artery disease and a rat model with femoral artery ligation, amplified SNA and BP responses to static exercise were observed. This dysfunction of the exercise pressor reflex has previously been shown to be mediated, in part, by muscle mechanoreflex overactivity. Thus, in this report, we determined whether kinin B2 receptor contributes to the augmented mechanoreflex activity in rats with 24 h of femoral artery occlusion. First, Western blot analysis was used to examine protein expression of B2 receptors in dorsal root ganglion tissues of control limbs and ligated limbs. Our data show that B2 receptor displays significant overexpression in ligated limbs as compared with control limbs (optical density: 0.94 ± 0.02 in control and 1.87 ± 0.08 after ligation, P < 0.05 vs. control; n = 6 in each group). Second, mechanoreflex was evoked by muscle stretch and the reflex renal SNA (RSNA) and mean arterial pressure (MAP) responses to muscle stretch were examined after HOE-140, a B2 receptors blocker, was injected into the arterial blood supply of the hindlimb muscles. The results demonstrate that the stretch-evoked reflex responses were attenuated by administration of HOE-140 in control rats and ligated rats; however, the attenuating effects of HOE-140 were significantly greater in ligated rats, i.e., after 5 μg/kg of HOE-140 RSNA and MAP responses evoked by 0.5 kg of muscle tension were attenuated by 43% and 25% in control vs. 54% and 34% in ligation ( P < 0.05 vs. control group; n = 11 in each group). In contrast, there was no significant difference in B1 receptor expression in both experimental groups, and arterial injection of R-715, a B1 receptors blocker, had no significant effects on RSNA and MAP responses evoked by muscle stretch. Accordingly, results obtained from this study support our hypothesis that heightened kinin B2 receptor expression in the sensory nerves contributes to the exaggerated muscle mechanoreflex in rats with femoral artery occlusion.

scholarly journals PPADS does not block contraction-induced prostaglandin E2 synthesis in cat skeletal muscle

2008 ◽  
Vol 295 (5) ◽  
pp. H2043-H2045 ◽  
Author(s):  
Jennifer L. McCord ◽  
Shawn G. Hayes ◽  
Marc P. Kaufman
Keyword(s):  
Skeletal Muscle ◽  
Pyridoxal Phosphate ◽  
Pressor Response ◽  
Triceps Surae ◽  
Prostaglandin E ◽  
Exercise Pressor Reflex ◽  
Before And After ◽  
Pressor Reflex ◽  
Response To Exercise

Pyridoxal-phosphate-6-azophenyl-2′-4-disulfonate (PPADS), a purinergic 2 (P2) receptor antagonist, has been shown to attenuate the exercise pressor reflex in cats. In vitro, however, PPADS has been shown to block the production of prostaglandins, some of which play a role in evoking the exercise pressor reflex. Thus the possibility exists that PPADS blocks the exercise pressor reflex through a reduction in prostaglandin synthesis rather than through the blockade of P2 receptors. Using microdialysis, we collected interstitial fluid from skeletal muscle to determine prostaglandin E2 (PGE2) concentrations during the intermittent contraction of the triceps surae muscle before and after a popliteal arterial injection of PPADS (10 mg/kg). We found that the PGE2 concentration increased in response to the intermittent contraction before and after the injection of PPADS (both, P < 0.05). PPADS reduced the pressor response to exercise ( P < 0.05) but had no effect on the magnitude of PGE2 production during contraction ( P = 0.48). These experiments demonstrate that PPADS does not block the exercise pressor reflex through a reduction in PGE2 synthesis. We suggest that PGE2 and P2 receptors play independent roles in stimulating 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.

Segmental effect of spinal NK-1 receptor blockade on the pressor reflex

1998 ◽  
Vol 275 (3) ◽  
pp. H789-H796 ◽  
Author(s):  
L. Britt Wilson ◽  
Gregory A. Hand
Keyword(s):  
Skeletal Muscle ◽  
Spinal Cord ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Pressor Response ◽  
Afferent Neurons ◽  
Muscle Stretch ◽  
Primary Afferent ◽  
Static Contraction ◽  
Pressor Reflex

The physiological effects of substance P (SP) are mediated via activation of neurokinin-1 (NK-1) receptors. The purpose of this study was to test the hypothesis that blockade of NK-1 receptors in the dorsal horn, both at the site of entry for the primary afferent neurons and adjacent spinal segments, attenuates the pressor reflex evoked by static contraction and stretch of skeletal muscle. Cats were anesthetized with α-chloralose and urethan, and a laminectomy was performed. With the exception of the L7 dorsal root, the dorsal and ventral roots from L5 to S2 were sectioned on one side of the spinal cord. Thus the primary afferent fibers mediating the pressor reflex enter the spinal cord via the L7 dorsal root in these experiments. Based on dose-response data, dialysis of the NK-1 receptor antagonist CP-96,345 (5 mM for 2 h) into the L7 dorsal horn ipsilateral to the contracting muscle attenuated the pressor response to static contraction (75 ± 15 vs. 46 ± 7 mmHg; n = 5 cats) but not muscle stretch (60 ± 12 vs. 50 ± 8 mmHg). Administration of the inactive enantiomer of CP-96,345, CP-96,344 (5 mM for 2 h), into the L7 dorsal horn failed to alter the cardiovascular changes elicited by contraction (45 ± 7 vs. 43 ± 6 mmHg) and stretch (31 ± 8 vs. 32 ± 11). Dialysis of 5 mM CP-96,345 into the dorsal horn at the L6 and S1 segments for 2 h decreased the peak pressor response to static contraction (58 ± 9 vs. 31 ± 6 mmHg; n = 7) and muscle stretch (61 ± 6 vs. 44 ± 8 mmHg). These data suggest that the activation of NK-1 receptors, both at the site of entry and in regions outside of the entry site for afferent neurons, is involved in the spinal processing that produces the pressor reflex evoked by static contraction of skeletal muscle.

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