Regulation of sympathetic tone and arterial pressure by rostral ventrolateral medulla after depletion of C1 cells in rat

In this study we examined whether the rostral ventrolateral medulla (RVLM) maintains resting sympathetic vasomotor tone and activates sympathetic nerve activity (SNA) after the depletion of bulbospinal C1 adrenergic neurones. Bulbospinal C1 cells were destroyed (≈84% loss) by bilateral microinject...

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Bibliographic Details
Published in:The Journal of physiology 2000-11, Vol.529 (1), p.221-236
Main Authors: Schreihofer, Ann M., Stornetta, Ruth L., Guyenet, Patrice G.
Format: Article
Language:English
Subjects:
Animals
Blood Pressure - physiology
Dopamine beta-Hydroxylase - antagonists & inhibitors
Electric Stimulation
Enzyme Inhibitors - pharmacology
GABA Agonists - administration & dosage
GABA Agonists - pharmacology
Hippocampus - cytology
Hippocampus - physiology
Immunohistochemistry
Immunotoxins
Male
Medulla Oblongata - physiology
Microinjections
Muscimol - administration & dosage
Muscimol - pharmacology
N-Glycosyl Hydrolases
Neurons - physiology
Original
Plant Proteins - administration & dosage
Plant Proteins - pharmacology
Rats
Rats, Sprague-Dawley
Ribosome Inactivating Proteins, Type 1
Saporins
Spinal Nerves - physiology
Sympathectomy, Chemical
Sympathetic Nervous System - cytology
Sympathetic Nervous System - physiology
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Summary:In this study we examined whether the rostral ventrolateral medulla (RVLM) maintains resting sympathetic vasomotor tone and activates sympathetic nerve activity (SNA) after the depletion of bulbospinal C1 adrenergic neurones. Bulbospinal C1 cells were destroyed (≈84% loss) by bilateral microinjections (spinal segments T 2 -T 3 ) of an anti-dopamine-β-hydroxylase antibody conjugated to the ribosomal toxin saporin (anti-DβH-SAP). Extracellular recording and juxtacellular labelling of bulbospinal barosensitive neurones in the RVLM revealed that treatment with anti-DβH-SAP spared the lightly myelinated neurones with no tyrosine hydroxylase immunoreactivity. In rats treated with anti-DβH-SAP, inhibition of RVLM neurones by bilateral microinjection of muscimol eliminated splanchnic SNA and produced the same degree of hypotension as in control rats. Following treatment with anti-DβH-SAP the sympathoexcitatory (splanchnic nerve) and pressor responses to electrical stimulation of the RVLM were reduced. Treatment with anti-DβH-SAP also eliminated the majority of A5 noradrenergic neurones. However, rats with selective lesion of A5 cells by microinjection of 6-hydroxydopamine into the pons showed no deficits to stimulation of the RVLM. In summary, the loss of 84% of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats, but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation. The data suggest sympathoexcitatory roles for both the C1 cells and non-C1 cells of the RVLM and further suggest the C1 cells are critical for the full expression of sympathoexcitatory responses generated by the RVLM.
ISSN:0022-3751
1469-7793
DOI:10.1111/j.1469-7793.2000.00221.x