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Functional Connections of the Vestibulo-spino-adrenal Axis in the Control of Blood Pressure Via the Vestibulosympathetic Reflex in Conscious Rats.

Lu HJ, Li MH, Li MZ, Park SE, Kim MS, Jin YZ, Park BR - Korean J. Physiol. Pharmacol. (2015)

Bottom Line: Significant evidence supports the role of the vestibular system in the regulation of blood pressure during postural movements.In the present study, the role of the vestibulo-spino-adrenal (VSA) axis in the modulation of blood pressure via the vestibulosympathetic reflex was clarified by immunohistochemical and enzyme immunoassay methods in conscious rats with sinoaortic denervation.These results indicate that the VSA axis may be a key component of the pathway used by the vestibulosympathetic reflex to maintain blood pressure during postural movements.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pathophysiology, Yanbian University College of Medicine and Key Laboratory of Natural Resources of Changbai Mountain & Functional Molecules at Yanbian University, Yanji 133002, China.

ABSTRACT
Significant evidence supports the role of the vestibular system in the regulation of blood pressure during postural movements. In the present study, the role of the vestibulo-spino-adrenal (VSA) axis in the modulation of blood pressure via the vestibulosympathetic reflex was clarified by immunohistochemical and enzyme immunoassay methods in conscious rats with sinoaortic denervation. Expression of c-Fos protein in the intermediolateral cell column of the middle thoracic spinal regions and blood epinephrine levels were investigated, following microinjection of glutamate receptor agonists or antagonists into the medial vestibular nucleus (MVN) and/or sodium nitroprusside (SNP)-induced hypotension. Both microinjection of glutamate receptor agonists (NMDA and AMPA) into the MVN or rostral ventrolateral medullary nucleus (RVLM) and SNP-induced hypotension led to increased number of c-Fos positive neurons in the intermediolateral cell column of the middle thoracic spinal regions and increased blood epinephrine levels. Pretreatment with microinjection of glutamate receptor antagonists (MK-801 and CNQX) into the MVN or RVLM prevented the increased number of c-Fos positive neurons resulting from SNP-induced hypotension, and reversed the increased blood epinephrine levels. These results indicate that the VSA axis may be a key component of the pathway used by the vestibulosympathetic reflex to maintain blood pressure during postural movements.

No MeSH data available.


Related in: MedlinePlus

Photomicrographs showing the effect of medial vestibular nucleus (MVN) glutamate on c-Fos protein expression in the spinal cord. (A) Effect of microinjection of glutamate receptor agonists into the left MVN on c-Fos protein expression in the intermediolateral cell column (IMC) of the T7 spinal cord. (B) Effect of pretreatment with microinjection of glutamate receptor antagonists into the left MVN on c-Fos protein expression in the IMC of the T7 spinal cord. Right lower quadrant in A and B represents higher magnification. Rectangles in right lower corner of each diagram represent higher magnification. ACSF, microinjection of artificial cerebrospinal fluid into the MVN; NMDA, microinjection of NMDA into the MVN; AMPA, microinjection of AMPA into the MVN; ACSF+SNP, SNP infusion after pretreatment with ACSF in the MVN; MK801+SNP, SNP infusion after pretreatment with MK801 in the MVN; CNQX+SNP, SNP infusion after pretreatment with CNQX in the MVN. ACSF, artificial cerebrospinal fluid; AMPA, 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl) propanoic acid; CNQX, 6-cyano-7-nitroquinoxaline-2,3-dione; IMC, intermediolateral cell column; MK801, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate; NMDA, N-methyl-D-aspartic acid; SNP, sodium nitroprusside.
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Figure 1: Photomicrographs showing the effect of medial vestibular nucleus (MVN) glutamate on c-Fos protein expression in the spinal cord. (A) Effect of microinjection of glutamate receptor agonists into the left MVN on c-Fos protein expression in the intermediolateral cell column (IMC) of the T7 spinal cord. (B) Effect of pretreatment with microinjection of glutamate receptor antagonists into the left MVN on c-Fos protein expression in the IMC of the T7 spinal cord. Right lower quadrant in A and B represents higher magnification. Rectangles in right lower corner of each diagram represent higher magnification. ACSF, microinjection of artificial cerebrospinal fluid into the MVN; NMDA, microinjection of NMDA into the MVN; AMPA, microinjection of AMPA into the MVN; ACSF+SNP, SNP infusion after pretreatment with ACSF in the MVN; MK801+SNP, SNP infusion after pretreatment with MK801 in the MVN; CNQX+SNP, SNP infusion after pretreatment with CNQX in the MVN. ACSF, artificial cerebrospinal fluid; AMPA, 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl) propanoic acid; CNQX, 6-cyano-7-nitroquinoxaline-2,3-dione; IMC, intermediolateral cell column; MK801, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate; NMDA, N-methyl-D-aspartic acid; SNP, sodium nitroprusside.

Mentions: The intermediolateral cell column in the T4-T7 spinal cord region did not show any expression of c-Fos protein under resting conditions in rats with intact baroreceptors and vestibular receptors. In addition, rats with SAD did not show any expression of c-Fos protein in the spinal cord under resting conditions. Expression of c-Fos protein in the intermediolateral cell column of the T4-T7 spinal cord was measured following drug modulation of MVN activity, in order to measure the functional connectivity between the MVN and the spinal cord. The number of c-Fos positive neurons in the intermediolateral cell column of the spinal cord was 2.2±1.0 in rats after microinjection of artificial cerebrospinal fluid (ACSF) into the MVN. However, microinjection of glutamate receptor agonists significantly increased the number of c-Fos positive neurons in the spinal cord as compared to ACSF microinjection. N-methyl-D-aspartic acid (NMDA) increased the number of c-Fos positive neurons to 20.5±2.2, and 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl) propanoic acid (AMPA) increased the number of c-Fos positive neurons to 21.8±1.9. The effect of glutamate receptor antagonists on the expression of c-Fos protein in the spinal cord was also investigated in rats with SNP-induced hypotension. SNP-induced hypotension increased the number of c-Fos positive neurons in the spinal cord to 27.0±3.9 as compared to the normotensive rat levels of 2.2±1.0, with both groups receiving microinjection of ACSF into the MVN. The effects of two glutamate receptor antagonists, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate (MK801) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), were then tested. Pretreatment with microinjection of either MK801 or CNQX into the MVN significantly decreased the number of c-Fos positive neurons in the spinal cord to 8.7±6.0 or 3.7±2.4, respectively, after SNP-induced hypotension as compared to the ACSF+SNP group (Fig. 1 and 2).


Functional Connections of the Vestibulo-spino-adrenal Axis in the Control of Blood Pressure Via the Vestibulosympathetic Reflex in Conscious Rats.

Lu HJ, Li MH, Li MZ, Park SE, Kim MS, Jin YZ, Park BR - Korean J. Physiol. Pharmacol. (2015)

Photomicrographs showing the effect of medial vestibular nucleus (MVN) glutamate on c-Fos protein expression in the spinal cord. (A) Effect of microinjection of glutamate receptor agonists into the left MVN on c-Fos protein expression in the intermediolateral cell column (IMC) of the T7 spinal cord. (B) Effect of pretreatment with microinjection of glutamate receptor antagonists into the left MVN on c-Fos protein expression in the IMC of the T7 spinal cord. Right lower quadrant in A and B represents higher magnification. Rectangles in right lower corner of each diagram represent higher magnification. ACSF, microinjection of artificial cerebrospinal fluid into the MVN; NMDA, microinjection of NMDA into the MVN; AMPA, microinjection of AMPA into the MVN; ACSF+SNP, SNP infusion after pretreatment with ACSF in the MVN; MK801+SNP, SNP infusion after pretreatment with MK801 in the MVN; CNQX+SNP, SNP infusion after pretreatment with CNQX in the MVN. ACSF, artificial cerebrospinal fluid; AMPA, 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl) propanoic acid; CNQX, 6-cyano-7-nitroquinoxaline-2,3-dione; IMC, intermediolateral cell column; MK801, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate; NMDA, N-methyl-D-aspartic acid; SNP, sodium nitroprusside.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
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Figure 1: Photomicrographs showing the effect of medial vestibular nucleus (MVN) glutamate on c-Fos protein expression in the spinal cord. (A) Effect of microinjection of glutamate receptor agonists into the left MVN on c-Fos protein expression in the intermediolateral cell column (IMC) of the T7 spinal cord. (B) Effect of pretreatment with microinjection of glutamate receptor antagonists into the left MVN on c-Fos protein expression in the IMC of the T7 spinal cord. Right lower quadrant in A and B represents higher magnification. Rectangles in right lower corner of each diagram represent higher magnification. ACSF, microinjection of artificial cerebrospinal fluid into the MVN; NMDA, microinjection of NMDA into the MVN; AMPA, microinjection of AMPA into the MVN; ACSF+SNP, SNP infusion after pretreatment with ACSF in the MVN; MK801+SNP, SNP infusion after pretreatment with MK801 in the MVN; CNQX+SNP, SNP infusion after pretreatment with CNQX in the MVN. ACSF, artificial cerebrospinal fluid; AMPA, 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl) propanoic acid; CNQX, 6-cyano-7-nitroquinoxaline-2,3-dione; IMC, intermediolateral cell column; MK801, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate; NMDA, N-methyl-D-aspartic acid; SNP, sodium nitroprusside.
Mentions: The intermediolateral cell column in the T4-T7 spinal cord region did not show any expression of c-Fos protein under resting conditions in rats with intact baroreceptors and vestibular receptors. In addition, rats with SAD did not show any expression of c-Fos protein in the spinal cord under resting conditions. Expression of c-Fos protein in the intermediolateral cell column of the T4-T7 spinal cord was measured following drug modulation of MVN activity, in order to measure the functional connectivity between the MVN and the spinal cord. The number of c-Fos positive neurons in the intermediolateral cell column of the spinal cord was 2.2±1.0 in rats after microinjection of artificial cerebrospinal fluid (ACSF) into the MVN. However, microinjection of glutamate receptor agonists significantly increased the number of c-Fos positive neurons in the spinal cord as compared to ACSF microinjection. N-methyl-D-aspartic acid (NMDA) increased the number of c-Fos positive neurons to 20.5±2.2, and 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl) propanoic acid (AMPA) increased the number of c-Fos positive neurons to 21.8±1.9. The effect of glutamate receptor antagonists on the expression of c-Fos protein in the spinal cord was also investigated in rats with SNP-induced hypotension. SNP-induced hypotension increased the number of c-Fos positive neurons in the spinal cord to 27.0±3.9 as compared to the normotensive rat levels of 2.2±1.0, with both groups receiving microinjection of ACSF into the MVN. The effects of two glutamate receptor antagonists, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate (MK801) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), were then tested. Pretreatment with microinjection of either MK801 or CNQX into the MVN significantly decreased the number of c-Fos positive neurons in the spinal cord to 8.7±6.0 or 3.7±2.4, respectively, after SNP-induced hypotension as compared to the ACSF+SNP group (Fig. 1 and 2).

Bottom Line: Significant evidence supports the role of the vestibular system in the regulation of blood pressure during postural movements.In the present study, the role of the vestibulo-spino-adrenal (VSA) axis in the modulation of blood pressure via the vestibulosympathetic reflex was clarified by immunohistochemical and enzyme immunoassay methods in conscious rats with sinoaortic denervation.These results indicate that the VSA axis may be a key component of the pathway used by the vestibulosympathetic reflex to maintain blood pressure during postural movements.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pathophysiology, Yanbian University College of Medicine and Key Laboratory of Natural Resources of Changbai Mountain & Functional Molecules at Yanbian University, Yanji 133002, China.

ABSTRACT
Significant evidence supports the role of the vestibular system in the regulation of blood pressure during postural movements. In the present study, the role of the vestibulo-spino-adrenal (VSA) axis in the modulation of blood pressure via the vestibulosympathetic reflex was clarified by immunohistochemical and enzyme immunoassay methods in conscious rats with sinoaortic denervation. Expression of c-Fos protein in the intermediolateral cell column of the middle thoracic spinal regions and blood epinephrine levels were investigated, following microinjection of glutamate receptor agonists or antagonists into the medial vestibular nucleus (MVN) and/or sodium nitroprusside (SNP)-induced hypotension. Both microinjection of glutamate receptor agonists (NMDA and AMPA) into the MVN or rostral ventrolateral medullary nucleus (RVLM) and SNP-induced hypotension led to increased number of c-Fos positive neurons in the intermediolateral cell column of the middle thoracic spinal regions and increased blood epinephrine levels. Pretreatment with microinjection of glutamate receptor antagonists (MK-801 and CNQX) into the MVN or RVLM prevented the increased number of c-Fos positive neurons resulting from SNP-induced hypotension, and reversed the increased blood epinephrine levels. These results indicate that the VSA axis may be a key component of the pathway used by the vestibulosympathetic reflex to maintain blood pressure during postural movements.

No MeSH data available.


Related in: MedlinePlus