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.

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.

NMDA receptor blockade in cat dorsal horn blunts reflex pressor response to muscle contraction and stretch

1996 ◽  
Vol 270 (2) ◽  
pp. H500-H508 ◽  
Author(s):  
G. A. Hand ◽  
A. F. Meintjes ◽  
A. W. Keister ◽  
A. Ally ◽  
L. B. Wilson
Keyword(s):  
Nmda Receptor ◽  
Muscle Contraction ◽  
Nmda Receptors ◽  
Dorsal Horn ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Nmda Receptor Antagonist ◽  
Muscle Afferents ◽  
The Central Nervous System ◽  
Passive Stretch

The role of N-methyl-D-aspartate (NMDA) receptors in the reflex pressor response to static muscle contraction and passive stretch was examined by microdialyzing the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate (AP-5) into the L7 or L6 and S1 levels of the dorsal horn of anesthetized cats. Contraction, elicited by electrical stimulation of the cut L7 and S1 ventral roots, increased mean arterial pressure (MAP) and heart rate (HR). Passive stretch at tensions similar to those generated by contraction also increased these variables. These cardiovascular changes were unaffected by dialyzing AP-5 (10 mM) into the dorsal horn at L7. Increasing the syringe concentration of AP-5 to 100 mM attenuated the pressor and HR responses from 62 +/- 8 to 31 +/- 6 mmHg and 18 +/- 4 to 12 +/- 4 beats/min, respectively. AP-5 blunted the increase in MAP (59 +/- 10 vs. 41 +/- 10 mmHg) evoked by muscle stretch. Simultaneously microdialyzing AP-5 (10 or 100 mM) into the dorsal horn at the L6 and S1 spinal levels also blunted the MAP and HR responses to contraction and stretch. These results suggest that NMDA receptors play a role in mediating the MAP and HR responses to static muscle contraction at the spinal level of the central nervous system. Furthermore, these data demonstrate that collaterals from muscle afferents partially mediate the reflex cardiovascular responses evoked by muscle contraction and stretch.

scholarly journals Cyclooxygenase inhibition does not impact the pressor response during static or dynamic mechanoreflex activation in healthy decerebrate rats

2019 ◽  
Vol 317 (3) ◽  
pp. R369-R378 ◽  
Author(s):  
Korynne S. Rollins ◽  
Tyler D. Hopkins ◽  
Alec L. Butenas ◽  
Kennedy P. Felice ◽  
Carl J. Ade ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Pressor Response ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Prostaglandin E ◽  
Muscle Stretch ◽  
Triceps Surae Muscle ◽  
Cox Inhibitor

Passive limb movement and limb muscle stretch in humans and animals are common experimental strategies used to investigate activation of the muscle mechanoreflex independent of contraction-induced metabolite production. Cyclooxygenase (COX) metabolites, however, are produced by skeletal muscle stretch in vitro and have been found to impact various models of mechanoreflex activation. Whether COX metabolites influence the decerebrate rat triceps surae muscle stretch mechanoreflex model remains unknown. We examined the effect of rat triceps surae muscle stretch on the interstitial concentration of the COX metabolite prostaglandin E2 (PGE2). Interstitial PGE2 concentration was increased above baseline values by 4 min of both static (38% increase, P = 0.01) and dynamic (56% increase, P < 0.01) triceps surae muscle stretch ( n = 10). The 4-min protocol was required to collect enough microdialysis fluid for PGE2 detection. The finding that skeletal muscle stretch in vivo was capable of producing COX metabolites prompted the hypothesis that intra-arterial administration of the COX inhibitor indomethacin (1 mg/kg) would reduce the pressor and cardioaccelerator responses evoked during 30 s (the duration most commonly used in the rat mechanoreflex model) of static and dynamic rat triceps surae muscle stretch. We found that indomethacin had no effect ( P > 0.05, n = 9) on the pressor or cardioaccelerator response during 30 s of either static or dynamic stretch. We conclude that, despite the possibility of increased COX metabolite concentration, COX metabolites do not activate or sensitize thin-fiber muscle afferents stimulated during 30 s of static or dynamic hindlimb skeletal muscle stretch in healthy rats.

Gadolinium attenuates exercise pressor reflex in cats

2001 ◽  
Vol 280 (5) ◽  
pp. H2153-H2161 ◽  
Author(s):  
Shawn G. Hayes ◽  
Marc P. Kaufman
Keyword(s):  
Pressor Response ◽  
Oxygen Demand ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Mechanical Stimuli ◽  
Group Iii ◽  
Exercise Pressor Reflex ◽  
Static Contraction ◽  
Pressor Reflex ◽  
Triceps Surae Muscles

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 α-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.

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.

Rostral ventrolateral medullary opioid receptor activation modulates pressor response to muscle contraction

1998 ◽  
Vol 274 (1) ◽  
pp. H139-H146 ◽  
Author(s):  
Daryl Caringi ◽  
David J. Mokler ◽  
David M. Koester ◽  
Ahmmed Ally
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Ventrolateral Medulla ◽  
Tibial Nerve Stimulation ◽  
Isometric Muscle Contraction ◽  
Isometric Muscle

The effects of an opioid agonist, [d-Ala2]methionine enkephalinamide (DAME), administered into the rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses to isometric muscle contraction were determined in anesthetized rats. A 30-s contraction evoked by tibial nerve stimulation increased mean arterial pressure (MAP) and heart rate (HR) by 34 ± 6 mmHg and 40 ± 7 beats/min, respectively, with a developed tension of 322 ± 30 g, after bilateral insertion of microdialysis probes into the rVLM. Thirty-minute dialysis of DAME (10 and 100 μM) attenuated the contraction-evoked cardiovascular changes dose dependently (10 μM: MAP = 25 ± 4 mmHg, HR = 27 ± 3 beats/min, tension = 333 ± 25 g; 100 μM: MAP = 14 ± 4 mmHg, HR = 16 ± 5 beats/min, tension = 330 ± 34 g). Preadministration of an opioid antagonist, naloxone (100 μM), augmented contraction-evoked MAP and HR responses and blocked effects of 100 μM DAME. Microdialysis of DAME into the cVLM produced no changes in the pressor response to contraction. At end of each experiment, tibial nerve stimulation after neuromuscular blockade evoked no MAP or HR change. Results demonstrate that opioid receptor activation within the rVLM modulates cardiovascular responses to isometric muscle contraction.

Effects of ventrolateral medullary AMPA-receptor antagonism on pressor response during muscle contraction

1997 ◽  
Vol 272 (6) ◽  
pp. H2774-H2781 ◽  
Author(s):  
T. Kobayashi ◽  
D. Caringi ◽  
D. J. Mokler ◽  
A. Ally
Keyword(s):  
Heart Rate ◽  
Muscle Contraction ◽  
Ampa Receptors ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Contrast Administration ◽  
Tibial Nerve Stimulation ◽  
Before And After

Effects of administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration that preferentially blocks alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors into rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses elicited during static muscle contraction were investigated using anesthetized rats. Two microdialysis probes were inserted bilaterally into either the rVLM or the cVLM using stereotaxic guides. A tibial nerve stimulation-evoked static muscle contraction for 30 s increased mean arterial pressure (MAP) and heart rate (HR) by 27 +/- 3 mmHg and 28 +/- 4 beats/min, respectively. Microdialysis of CNQX into the rVLM for 30 min attenuated the contraction-evoked increases in MAP and HR (10 +/- 2 mmHg and 12 +/- 2 beats/min). Developed tensions were similar during the contractions before and after microdialyzing CNQX. In contrast, administration of CNQX into the cVLM potentiated the muscle contraction-evoked cardiovascular responses (MAP, 25 +/- 4 vs. 39 +/- 6 mmHg; HR, 27 +/- 3 vs. 42 +/- 3 beats/min), with no change in developed tensions. Results demonstrate that AMPA receptors within the rVLM and the cVLM appear to play opposite modulatory roles in the central integration of cardiovascular responses elicited during static muscle contraction.

Cardiovascular responses during feeding in newborn lambs

1989 ◽  
Vol 257 (3) ◽  
pp. R568-R573
Author(s):  
B. L. Langille ◽  
S. L. Adamson ◽  
S. A. Jones
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Gastrointestinal Tract ◽  
Pressor Response ◽  
Sympathetic Innervation ◽  
Cardiovascular Responses ◽  
Bottle Feeding ◽  
Chemical Sympathectomy ◽  
Thyroid Glands ◽  
6 Hydroxydopamine

We examined the cardiovascular responses to bottle feeding in newborn lambs. Feeding induced a persistent rise in blood pressure, from 76.3 +/- 1.9 mmHg to 114 +/- 3.8 mmHg, that lasted for the duration of the feeding episode. This was accompanied by a transient tachycardia that lasted for approximately 10 s at the beginning of each feeding episode. Vasoconstriction of the hindlimb circulation, the gastrointestinal tract, kidneys, and adrenal and thyroid glands contributed to the pressor response, whereas changes in skeletal muscle resistance were not statistically significant. Of tissues assessed, only those actively involved in feeding (tongue and esophagus) vasodilated. Feeding tachycardia was greatly inhibited or abolished by the beta-blocker propranolol but the alpha-blocker phentolamine caused only moderate inhibition of the pressor response. Furthermore, chemical sympathectomy with 6-hydroxydopamine delayed the onset of the pressor response but did not abolish the ultimate rise in pressure. These findings indicate that feeding causes a significant pressor response in newborn lambs that is only partially mediated by sympathetic innervation.

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.

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