Activation of Spinobulbar Lamina I Neurons by Static Muscle Contraction

2002 ◽  
Vol 87 (3) ◽  
pp. 1641-1645 ◽  
Author(s):  
L. B. Wilson ◽  
D. Andrew ◽  
A. D. Craig
Keyword(s):  
Muscle Contraction ◽  
Small Diameter ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Ventrolateral Medulla ◽  
Antidromic Activation ◽  
Lamina I ◽  
Arterial Blood ◽  
Autonomic Reflexes ◽  
Blood Pressure Responses

Spinal lamina I neurons are selectively activated by small-diameter somatic afferents, and they project to brain stem sites that are critical for homeostatic control. Because small-diameter afferent activity evoked by contraction of skeletal muscle reflexly elicits exercise-related cardiorespiratory activation, we tested whether spinobulbar lamina I cells respond to muscle contraction. Spinobulbar lamina I neurons were identified in chloralose-anesthetized cats by antidromic activation from the ipsilateral caudal ventrolateral medulla. Static contractions of the ipsilateral triceps surae muscle were evoked by tibial nerve stimulation using parameters that avoid afferent activation, and arterial blood pressure responses were recorded. Recordings were maintained from 13 of 17 L7 lamina I spinobulbar neurons during static muscle contraction, and 5 of these neurons were excited. Three were selectively activated only by muscle afferents and did not have a cutaneous receptive field. Spinobulbar lamina I neurons activated by muscle contraction provide an ascending link for the reflex cardiorespiratory adjustments that accompany muscular work. This study provides an important first step in elucidating an ascending afferent pathway for somato-autonomic reflexes.

Cardiovascular and renal nerve responses to static muscle contraction of decerebrate rabbits

1994 ◽  
Vol 77 (5) ◽  
pp. 2449-2455 ◽  
Author(s):  
L. B. Wilson ◽  
C. K. Dyke ◽  
J. A. Pawelczyk ◽  
P. T. Wall ◽  
J. H. Mitchell
Keyword(s):  
Blood Pressure ◽  
Muscle Contraction ◽  
Arterial Blood Pressure ◽  
Triceps Surae ◽  
Sympathetic Outflow ◽  
Subsequent Increase ◽  
Renal Nerve ◽  
Arterial Blood ◽  
Initial Decrease ◽  
Blood Pressure Responses

The purpose of this study was to determine whether the biphasic arterial blood pressure responses elicited by static muscle contraction of decerebrate rabbits are mediated, at least in part, by an initial decrease and a subsequent increase in sympathetic outflow. Renal sympathetic nerve activity (RSNA) was used as an index of sympathetic outflow. Static contraction of the triceps surae muscle (n = 14) initially decreased mean arterial blood pressure (MAP) -20 +/- 3 mmHg and heart rate (HR) -15 +/- 5 beats/min (nadir values). After this initial decrease, MAP increased 12 +/- 2 mmHg (peak increase) above baseline and there was a tendency for HR to be elevated (6 +/- 3 beats/min). The changes in RSNA during muscle contraction (n = 6) mirrored the nadir and peak responses of MAP (-50 +/- 9 and 32 +/- 11%). Muscle stretch (n = 11) also evoked similar nadir and peak responses of MAP (-20 +/- 5 and 9 +/- 1 mmHg), HR (-17 +/- 7 and 3 +/- 3 beats/min), and RSNA (-43 +/- 9 and 46 +/- 15%). These data suggest that the initial depressor and subsequent pressor responses elicited by skeletal muscle contraction and stretch are mediated, at least in part, by biphasic changes in sympathetic outflow.

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.

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.

Effects of muscle fatigue on mechanically sensitive afferents of slow conduction velocity in the cat triceps surae

1991 ◽  
Vol 65 (2) ◽  
pp. 360-370 ◽  
Author(s):  
L. Hayward ◽  
U. Wesselmann ◽  
W. Z. Rymer
Keyword(s):  
Muscle Contraction ◽  
Muscle Fatigue ◽  
Surface Pressure ◽  
Muscular Contraction ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Spontaneous Discharge ◽  
Primary Role ◽  
Mechanical Stimuli ◽  
Group Iii

1. Group III and IV muscle afferents have been shown to be sensitive to both mechanical stimuli and metabolic and thermal changes in muscle. To establish the potential role of slowly conducting muscle afferents in regulating motor output during fatigue, we recorded from mechanically sensitive group III and nonspindle group II afferents originating in the triceps surae in barbiturate-anesthetized cats. We evaluated the response of these afferents to tetanic muscle contraction, stretch, and surface pressure, before, during, and after fatigue. 2. Our results show that muscle fatigue both increases spontaneous discharge in these mechanically sensitive afferents and sensitizes their response to muscle stretch, surface pressure, and, in a few instances, muscle contraction. These fatigue-induced changes typically occurred after 5-10 min of submaximal fatiguing stimulation. 3. During recovery from muscle fatigue, several contraction-sensitive free nerve endings, which had become sensitized to contractions during fatigue, remained sensitized after 20-30 min of rest. 4. The results of this study provide support for the hypothesis that fatigue-induced excitation of slowly conducting afferents is significant in mediating fatigue-induced inhibition of motoneuron output. However, our finding that the discharge of many slowly conducting mechanoreceptor afferents declines during the initial phase of fatigue argues against a primary role for these afferents in mediating the initial decline in motoneuron rate that is so prominent in fatiguing maximum voluntary muscular contraction.

NO formation in nucleus tractus solitarii attenuates pressor response evoked by skeletal muscle afferents

2001 ◽  
Vol 280 (5) ◽  
pp. H2371-H2379 ◽  
Author(s):  
Jianhua Li ◽  
Jeffrey T. Potts
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Pressor Response ◽  
Extracellular Fluid ◽  
Cardiovascular Responses ◽  
Muscle Afferents ◽  
Nucleus Tractus Solitarii ◽  
Triceps Surae ◽  
No Formation ◽  
Fos Protein

We have previously shown that static muscle contraction induces the expression of c-Fos protein in neurons of the nucleus tractus solitarii (NTS) and that some of these cells were codistributed with neuronal NADPH-diaphorase [nitric oxide (NO) synthase]-positive fibers. In the present study, we sought to determine the role of NO in the NTS in mediating the cardiovascular responses elicited by skeletal muscle afferent fibers. Static contraction of the triceps surae muscle was induced by electrical stimulation of the L7 and S1 ventral roots in anesthetized cats. Muscle contraction during microdialysis of artificial extracellular fluid increased mean arterial pressure (MAP) and heart rate (HR) 51 ± 9 mmHg and 18 ± 3 beats/min, respectively. Microdialysis ofl-arginine (10 mM) into the NTS to locally increase NO formation attenuated the increases in MAP (30 ± 7 mmHg, P < 0.05) and HR (14 ± 2 beats/min, P > 0.05) during contraction. Microdialysis ofd-arginine (10 mM) did not alter the cardiovascular responses evoked by muscle contraction. Microdialysis of N G-nitro-l-arginine methyl ester (2 mM) during contraction attenuated the effects ofl-arginine on the reflex cardiovascular responses. These findings demonstrate that an increase in NO formation in the NTS attenuates the pressor response to static muscle contraction, indicating that the NO system plays a role in mediating the cardiovascular responses to static muscle contraction in the NTS.

Temperature modulates P2X receptor-mediated cardiovascular responses to muscle afferent activation

2006 ◽  
Vol 291 (3) ◽  
pp. H1255-H1261 ◽  
Author(s):  
Zhaohui Gao ◽  
Valerie Kehoe ◽  
Jihong Xing ◽  
Lawrence Sinoway ◽  
Jianhua Li
Keyword(s):  
Muscle Contraction ◽  
Atp Release ◽  
Cardiovascular Responses ◽  
P2x Receptors ◽  
Muscle Afferents ◽  
P2x Receptor ◽  
Muscle Temperature ◽  
Muscle Stretch ◽  
Arterial Blood ◽  
Muscle Afferent

Static muscle contraction increases ATP release into the muscle interstitial space. Elevated ATP in muscle stimulates thin fiber muscle afferents and increases blood pressure via engagement of purinergic P2X receptors. In addition, ATP activates P2X receptors and enhances cardiovascular responses induced by stimulation of muscle mechanoreceptors. In this study, we examined whether elevated muscle temperature would attenuate and whether reduced temperature would potentiate P2X effects on reflex muscle responses. α,β-Methylene ATP (α,β-MeATP) was injected into the arterial blood supply of hindlimb muscle to stimulate P2X receptors, and muscle stretch was induced to activate mechanically sensitive muscle afferents as α,β-MeATP was injected in 10 anesthetized cats. Femoral arterial injection of α,β-MeATP (1.0 mM) increased mean arterial pressure (MAP) by 35 ± 5 (35°C), 26 ± 3 (37°C), and 19 ± 3 mmHg (39°C; P < 0.05 vs. 35°C), respectively. Muscle stretch (2 kg) elevated MAP. The MAP response was significantly enhanced 34% and 36% when α,β-MeATP (0.2 mM) was arterially infused 5 min before muscle stretch at 35° and 37°C, respectively. However, as muscle temperature reached 39°C, the stretch-evoked response was augmented only 6% by α,β-MeATP injection, and the response was significantly attenuated compared with the response with muscle temperature of 35° and 37°C. In addition, we also examined effects of muscle temperature on α,β-MeATP enhancement of the cardiovascular responses to static muscle contraction while the muscles were freely perfused and the circulation to the muscles was occluded. Because muscle temperature was 37°C, arterial injections of α,β-MeATP significantly augmented contraction-evoked MAP response by 49% (freely perfused) and 53% (ischemic condition), respectively. It is noted that this effect was significantly attenuated at a muscle temperature of 39°C. These data indicate that the effect of P2X receptor on reflex muscle response is sensitive to alternations of muscle temperature and that elevated temperature attenuates the response.

Muscle pressor reflex: potential role of vanilloid type 1 receptor and acid-sensing ion channel

2004 ◽  
Vol 97 (5) ◽  
pp. 1709-1714 ◽  
Author(s):  
Jianhua Li ◽  
Michael D. Maile ◽  
Adam N. Sinoway ◽  
Lawrence I. Sinoway
Keyword(s):  
Cardiovascular Responses ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Reflex Response ◽  
Arterial Blood ◽  
Afferent Nerves ◽  
Muscle Afferent ◽  
Pressor Reflex ◽  
Stimulation Of

Reflex cardiovascular responses to muscle contraction are mediated by mechanical and metabolic stimulation of thin muscle afferent fibers. Metabolic stimulants and receptors involved in responses are uncertain. Capsaicin depolarizes thin sensory afferent nerves that have vanilloid type 1 receptors (VR1). Among potential endogenous ligands of thin fibers, H+ has been suggested as a metabolite mediating the reflex muscle response as well as a potential stimulant of VR1. It has also been suggested that acid-sensing ion channels (ASIC) mediate H+, evoking afferent nerve excitation. We have examined the roles of VR1 and ASIC in mediating cardiovascular reflex responses to acid stimulation of muscle afferents in a rat model. In anesthetized rats, injections of capsaicin into the arterial blood supply of triceps surae muscles evoked a biphasic response ( n = 6). An initial fall in mean arterial pressure (from baseline of 95.8 ± 9.5 to 70.4 ± 4.5 mmHg, P < 0.05 vs. baseline) was followed by an increase (to 131.6 ± 11.3 mmHg, P < 0.05 vs. baseline). Anandamide (an endogenous substance that activates VR1) induced the same change in blood pressure as did capsaicin. The pressor (but not depressor) component of the response was blocked by capsazepine (a VR1 antagonist) and section of afferent nerves. In decerebrate rats ( n = 8), H+ evoked a pressor response that was not blocked by capsazepine but was attenuated by amiloride (an ASIC blocker). In rats ( n = 12) pretreated with resiniferatoxin to destroy muscle afferents containing VR1, capsaicin and H+ responses were blunted. We conclude that H+ stimulates ASIC, evoking the reflex response, and that ASIC are likely to be frequently found on afferents containing VR1. The data also suggest that VR1 and ASIC may play a role in processing of muscle afferent signals, evoking the muscle pressor reflex.

Extracellular serotonin changes in VLM during muscle contraction: effects of 5-HT1A-receptor activation

1997 ◽  
Vol 273 (6) ◽  
pp. H2899-H2909 ◽  
Author(s):  
Gudbjorn Asmundsson ◽  
Daryl Caringi ◽  
David J. Mokler ◽  
Toshio Kobayashi ◽  
Takeshi Ishide ◽  
...  
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Tibial Nerve ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Ventrolateral Medulla ◽  
Muscle Paralysis ◽  
Arterial Blood ◽  
Tibial Nerve Stimulation ◽  
Static Contraction

This study determined whether muscle contraction causes an increase in extracellular levels of serotonin (5-HT) in the rostral (rVLM) or caudal ventrolateral medulla (cVLM) in anesthetized rats. Muscle contraction, evoked by tibial nerve stimulation, increased mean arterial blood pressure (MAP) by 27 ± 4 mmHg ( n = 8). In addition, 5-HT levels in the rVLM were elevated by 65 ± 9% during the contraction ( n = 8). Results were similar over two repeated contractions. In contrast, muscle contraction increased MAP, but not 5-HT, levels in the cVLM ( n = 6). Tibial nerve stimulation after muscle paralysis had no effect on either MAP or 5-HT levels in both rVLM and cVLM. Microdialysis of a 5-HT1A agonist, 8-OH-DPAT (10 mM), into the rVLM for 30 min ( n = 6) blunted the MAP change and reduced 5-HT release during contraction. Administration of NAN-190, a 5-HT1A antagonist, into the rVLM had no effect on 5-HT release and cardiovascular responses during muscle contraction and blocked the changes in 5-HT, MAP, and heart rate to static contraction after subsequent microdialysis of 8-OH-DPAT. Results demonstrate that 5-HT levels in the rVLM increase during muscle contraction and that 5-HT1A-receptor activation in the rVLM blunts MAP response to muscle contraction via a decrease in the extracellular concentration of 5-HT.

Cardiovascular effects of opioid antagonist naloxone in rostral ventrolateral medulla of rabbits

1990 ◽  
Vol 258 (2) ◽  
pp. R325-R331 ◽  
Author(s):  
D. A. Morilak ◽  
G. Drolet ◽  
J. Chalmers
Keyword(s):  
Pressor Response ◽  
Cardiovascular Effects ◽  
Rostral Ventrolateral Medulla ◽  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Ventrolateral Medulla ◽  
Inhibitory Influence ◽  
Beneficial Effects ◽  
Arterial Blood ◽  
Depressor Effect

We have examined the influence of endogenous opioids on the basal and reflex control of arterial blood pressure in the pressor region of the rostral ventrolateral medulla (RVLM) of chloralose-anesthetized rabbits. We tested basal effects both in intact animals and after hypotensive hemorrhage. Bilateral administration of the opiod antagonist naloxone (20 nmol, 100 nl) directly into the RVLM induced a gradual and prolonged increase in mean arterial pressure (MAP) (+17 +/- 2 mmHg). This was preceded by a brief and mild depressor effect (-9 +/- 3 mmHg), which was attributable to a transient reduction in excitability immediately after naloxone injection. When naloxone was administered into the RVLM after hemorrhage (20 ml/kg), it improved recovery of MAP relative to saline controls, again producing a gradual, prolonged pressor response (+29 +/- 5 mmHg). The effect of naloxone on a baroreflex in intact animals was only transient, with a brief, nonsignificant attenuation of the reflex depressor response to aortic nerve stimulation. We conclude that endogenous opioids exert a tonic inhibitory influence on RVLM pressor neurons and that this input remains active after hemorrhage. The RVLM may thus be one site for the beneficial effects of naloxone in preventing circulatory decompensation after hemorrhage. In contrast, opioid neurons are not an essential component of baroreflex-mediated sympathoinhibition in the RVLM.

scholarly journals Bradykinin Contributes to Sympathetic and Pressor Responses Evoked by Activation of Skeletal Muscle Afferents P2X in Heart Failure

2016 ◽  
Vol 39 (6) ◽  
pp. 2101-2109 ◽  
Author(s):  
Jihong Xing ◽  
Jianhua Li
Keyword(s):  
Heart Failure ◽  
Nervous Activity ◽  
Muscle Afferents ◽  
Receptor Expression ◽  
Sympathetic Nervous Activity ◽  
Published Data ◽  
Drg Neurons ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Muscle Afferent

Background/Aims: Published data suggest that purinergic P2X receptors of muscle afferent nerves contribute to the enhanced sympathetic nervous activity (SNA) and blood pressure (BP) responses during static exercise in heart failure (HF). In this study, we examined engagement of bradykinin (BK) in regulating responses of SNA and BP evoked by P2X stimulation in rats with HF. We further examined cellular mechanisms responsible for BK. We hypothesized that BK potentiates P2X currents of muscle dorsal root ganglion (DRG) neurons, and this effect is greater in HF due to upregulation of BK kinin B2 and P2X3 receptor. As a result, BK amplifies muscle afferents P2X-mediated SNA and BP responses. Methods: Renal SNA and BP responses were recorded in control rats and rats with HF. Western Blot analysis and patch-clamp methods were employed to examine the receptor expression and function of DRG neurons involved in the effects of BK. Results: BK injected into the arterial blood supply of the hindlimb muscles heightened the reflex SNA and BP responses induced by P2X activation with α,β-methylene ATP to a greater degree in HF rats. In addition, HF upregulated the protein expression of kinin B2 and P2X3 in DRG and the prior application of BK increased the magnitude of α,β-methylene ATP-induced currents in muscle DRG neurons from HF rats. Conclusion: BK plays a facilitating role in modulating muscle afferent P2X-engaged reflex sympathetic and pressor responses. In HF, P2X responsivness is augmented due to increases in expression of kinin B2 and P2X3 receptors and P2X current activity.

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