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

1995 ◽  
Vol 268 (6) ◽  
pp. R1464-R1471 ◽  
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.

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.

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

1997 ◽  
Vol 272 (4) ◽  
pp. R1020-R1027 ◽  
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.

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.

Inhibition of rostral VLM by baroreceptor activation is relayed through caudal VLM

1990 ◽  
Vol 258 (5) ◽  
pp. R1271-R1278 ◽  
Author(s):  
S. K. Agarwal ◽  
A. J. Gelsema ◽  
F. R. Calaresu
Keyword(s):  
Kynurenic Acid ◽  
Cardiac Cycle ◽  
Pressor Response ◽  
Inhibitory Response ◽  
Firing Frequency ◽  
Ventrolateral Medulla ◽  
Cardiovascular Neurons ◽  
Baroreceptor Activation ◽  
Acid Administration ◽  
Stimulation Of

Experiments were done to test the hypothesis that inhibition of neurons in the rostral ventrolateral medulla (RVLM) elicited by stimulation of the nucleus tractus solitarii (NTS) is relayed through the caudal ventrolateral medulla (CVLM). We recorded activity from 56 spontaneously firing units in the right RVLM of urethan-anesthetized and artificially ventilated rats. Eleven of these units were classified as cardiovascular neurons, because they were silenced by baroreceptor activation (1-3 micrograms phenylephrine iv) and showed rhythmicity of their spontaneous activity in synchrony with the cardiac cycle. Single pulses (0.1 ms, 30-75 microA) delivered 1/s to depressor sites in the ipsilateral NTS inhibited the activity of all these cardiovascular neurons. Microinjection of the glutamate antagonist kynurenic acid (0.15 M, 50 nl) into the ipsilateral CVLM blocked the inhibitory response of RVLM units to the administration of phenylephrine and increased the firing frequency of cardiovascular neurons in the RVLM by 43%. Moreover, kynurenic acid administration attenuated the inhibitory response of cardiovascular neurons in the RVLM to NTS stimulation. Finally, stimulation of the NTS that elicited depressor responses under control conditions produced a pressor response after kynurenic acid administration. The remaining 45 RVLM neurons were barosensitive but lacked cardiac cycle-related rhythmicity. These results provide direct evidence for the existence of a tonic inhibitory pathway from NTS to RVLM that is relayed through the CVLM probably by a glutamatergic projection from NTS to CVLM.

Involvement of the ventrolateral medulla in the mediation of pressor responses of the rat to afferent vagal stimulation

1985 ◽  
Vol 63 (12) ◽  
pp. 1612-1614 ◽  
Author(s):  
T. Kubo
Keyword(s):  
Spinal Cord ◽  
Vagal Stimulation ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Vasopressin Antagonist ◽  
Caudal Ventrolateral Medulla ◽  
Pressor Responses ◽  
Electrolytic Lesions ◽  
Afferent Vagal ◽  
Stimulation Of

Electrical stimulation of afferent vagal fibres evoked a pressor response in rats after transection of the spinal cord. The pressor response was accounted for by an increased release of vasopressin because it was abolished by the intravenous injection of a vasopressin antagonist. Bilateral electrolytic lesions at the sites of the caudal ventrolateral medulla markedly reduced the pressor response to afferent vagal stimulation but not that to carotid occlusion. It is concluded that the area of the caudal ventrolateral medulla is involved in mediation of the vasopressin-induced pressor response to afferent vagal stimulation.

Somatic and visceral inputs to neurons of the rostral ventrolateral medulla

1993 ◽  
Vol 265 (1) ◽  
pp. R35-R40 ◽  
Author(s):  
R. Ermirio ◽  
P. Ruggeri ◽  
C. Molinari ◽  
L. C. Weaver
Keyword(s):  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Renal Nerve ◽  
Afferent Stimulation ◽  
Cardiovascular Neurons ◽  
Sciatic Nerve Stimulation ◽  
Regulation Of Blood Pressure ◽  
Stimulation Of

Sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) play an essential role in the generation of basal sympathetic tone and in the reflex regulation of blood pressure. In this study responses of RVLM "cardiovascular" neurons to somatic and visceral afferent stimulation were investigated. The activity of 34 RVLM neurons was recorded in urethan-anesthetized paralyzed and artificially ventilated rats. These neurons were identified as cardiovascular based on their baroreceptor sensitivity and their pulse-synchronous discharge. Electrical stimulation of the sciatic nerve excited 31 of the 34 RVLM units (91%). Renal nerve stimulation inhibited firing of 14 of 22 RVLM neurons tested (64%), not affecting the remaining 8 units. Stimulation of splenic nerves inhibited the discharge of 7 of 12 RVLM neurons tested (58%), whereas the remaining 5 units were not affected. All RVLM units responsive to visceral afferent stimulation were also responsive to sciatic nerve stimulation. These results indicate that RVLM cardiovascular neurons receive somatic and visceral inputs, suggesting an involvement of these units in the integration of homeostatic responses to changes in the internal and external environment.

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.

Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

Effects of insulin on the cardiovascular integrating mechanisms of brain stem in cats

1993 ◽  
Vol 265 (4) ◽  
pp. E609-E616 ◽  
Author(s):  
S. W. Kuo ◽  
J. H. Hsieh ◽  
W. C. Wu ◽  
H. T. Horng ◽  
L. R. Shian ◽  
...  
Keyword(s):  
Brain Stem ◽  
Cardiovascular Responses ◽  
Serum Glucose ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Motor Nucleus ◽  
Renal Nerve ◽  
Pressor Responses ◽  
The Brain ◽  
Stimulation Of

In 65 cats anesthetized with alpha-chloralose and urethane, the effects of insulin on cardiovascular responses to stimulation of various structures in the brain stem were studied. The threshold dose of insulin injected intravenously that produced systemic hypoglycemia was 5-10 U/kg. Subthreshold hypoglycemic doses of insulin were used intracerebroventricularly (0.25 U/kg) or intracerebrally (2 mU in 200 nl). Sixty minutes after intravenous insulin, when serum glucose concentrations decreased from 158 to 43 mg/100 ml, pressor responses to stimulation of the periaqueductal gray of midbrain (PAG), locus coeruleus (LC), dorsal medulla (DM), ventrolateral medulla (VLM), and parvocellular reticular nucleus (PVC) decreased significantly. Depressor and bradycardiac response to stimulation of paramedian reticular nucleus or dorsal motor nucleus of vagus (DMV) decreased significantly as well. Thirty minutes after intracerebroventricular insulin, pressor responses of PAG, DM, and the bradycardiac response of DMV decreased significantly. Thirty minutes after intracerebral insulin, pressor responses and renal nerve activities of LC (but not PAG), VLM, DM, and PVC decreased significantly. A similar but faster onset (5 min) of depression of cardiovascular responses on stimulating the LC, VLM, DM, and PVC was observed in another six acutely midcollicular-decerebrate cats recovered from halothane anesthesia. These findings suggest that insulin directly inhibits the vasomotor structures of the brain stem and decreases the pressor responses to stimulation.

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