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

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.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.273.6.h2899 ◽

1997 ◽

Vol 273 (6) ◽

pp. H2899-H2909 ◽

Cited By ~ 4

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.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.6.h2774 ◽

1997 ◽

Vol 272 (6) ◽

pp. H2774-H2781 ◽

Cited By ~ 6

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.

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Central 5-HT1A modulation of cardiovascular responses to tibial nerve stimulation-evoked muscle contraction

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.272.4.r1020 ◽

1997 ◽

Vol 272 (4) ◽

pp. R1020-R1027 ◽

Cited By ~ 6

Author(s):

A. Ally ◽

D. Caringi ◽

D. M. Koester ◽

T. Kobayashi ◽

D. J. Mokler

Keyword(s):

Muscle Contraction ◽

Nerve Stimulation ◽

Tibial Nerve ◽

Muscle Tension ◽

Cardiovascular Responses ◽

Ventrolateral Medulla ◽

Motor Threshold ◽

Tibial Nerve Stimulation ◽

Prior Administration ◽

Stimulation Of

The effects of administering 8-hydroxy-2-(di-n-propylamine) tetralin [8-OH-DPAT, a serotonin 1A (5-HT1A) receptor agonist] into the rostral ventrolateral medulla (RVLM) on cardiovascular responses during tibial nerve stimulation-evoked muscle contraction were investigated using anesthetized rats. Stimulation of the tibial nerve (3 times motor threshold, 0.1 ms, 40 Hz) for 30 s increased mean arterial pressure (MAP), heart rate (HR), and muscle tension by 25 +/- 3 mmHg, 24 +/- 4 beats/min, and 299 +/- 35 g, respectively. Bilateral microdialysis of 8-OH-DPAT (10 mM) for 30 min attenuated the stimulation-evoked increases in MAP (8 +/- 2 mmHg) and HR (11 +/- 5 beats/min), without a change in muscle tension (292 +/- 30 g). However, administration of 1 mM 8-OH-DPAT had no effect on the cardiovascular responses. Thirty minutes of microdialysis of 8-OH-DPAT (10 mM) into the caudal ventrolateral medulla produced no effect on cardiovascular responses during muscle contraction. Prior administration of 10 mM 1-[2-methoxyphenyl]-4-[4-(2-phthalimido)-butyl]piperazine (NAN-190), a 5-HT1A receptor antagonist, for 30 min into the RVLM blocked the attenuating effects of subsequent microdialysis of 8-OH-DPAT (10 mM). Results suggest that activation of 5-HT1A receptors within the RVLM inhibit cardiovascular responses elicited during static muscle contraction.

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Role of ventrolateral medulla in reflex cardiovascular responses to activation of skin and muscle nerves

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.268.6.r1464 ◽

1995 ◽

Vol 268 (6) ◽

pp. R1464-R1471 ◽

Cited By ~ 2

Author(s):

P. Ruggeri ◽

R. Ermirio ◽

C. Molinari ◽

F. R. Calaresu

Keyword(s):

Nerve Stimulation ◽

Sural Nerve ◽

Tibial Nerve ◽

Pressor Response ◽

Cardiovascular Responses ◽

Ventrolateral Medulla ◽

Electrolytic Lesions ◽

Cardiovascular Neurons ◽

Muscle Nerve ◽

Stimulation Of

Central neuronal circuits mediating reflex cardiovascular responses to skin and muscle nerve stimulation were studied in rats under urethan anesthesia. Responses of right rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM) cardiovascular neurons to stimulation of contralateral skin and muscle afferent fibers were investigated. Stimulation of the tibial (muscle) nerve excited 19 (86%) of 22 CVLM neurons and inhibited 18 (82%) of 22 RVLM neurons. Stimulation of the sural (skin) nerve excited 20 (91%) of the 22 RVLM neurons but did not affect the firing rate of any of the 22 CVLM neurons. Electrolytic lesions of the CVLM abolished the depressor responses induced by stimulation of the tibial nerve without affecting the pressor response caused by sural nerve stimulation. Similarly, reversible blockade of the CVLM by microinjection of gamma-amino-butyric acid or CoCl2 abolished the depressor response to stimulation of the tibial nerve without affecting the pressor response induced by sural nerve stimulation. These results suggest that vasodepressor responses to muscle nerve activation are mediated by a neuronal inhibitory pathway to the RVLM relayed through the CVLM.

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