Baroreflex dependent and independent roles of the caudal ventrolateral medulla in cardiovascular regulation

Alan F. Sved, Satoru Ito, Christopher (Chris) Madden

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

The caudal ventrolateral medulla (CVLM) plays a critical role in cardiovascular regulation. Convincing data now support the hypothesis that inhibition of sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) by CVLM neurons constitutes the necessary inhibitory link in baroreceptor reflex mediated control of sympathetic vasomotor outflow. Inhibition or destruction of the CVLM produces severe acute hypertension, consistent with blockade of baroreceptor reflexes and withdrawal of inhibition of RVLM sympathoexcitatory neurons. However, other data indicate that the CVLM also tonically inhibits RVLM sympathoexcitatory neurons in a manner not driven by baroreceptor input. In some studies, inhibition of the CVLM results in an increase in arterial pressure (AP) without inhibiting baroreceptor reflexes, possibly reflecting baroreceptor-independent and baroreceptor-dependent sub-regions of the CVLM. Furthermore, in baroreceptor- denervated rats, inhibition of the CVLM still leads to large increases in AP. In addition, in spontaneously hypertensive rats (SHR) central processing of baroreceptor reflexes appears normal but CVLM-mediated inhibition of the RVLM seems to be attenuated, suggesting that it is specifically a baroreceptor- independent mechanism of cardiovascular regulation in SHR that is altered. Taken together, these findings support an important, tonic, baroreceptor- independent inhibition of RVLM sympathoexcitatory neurons exerted by the CVLM. (C) 2000 Elsevier Science Inc.

Original languageEnglish (US)
Pages (from-to)129-133
Number of pages5
JournalBrain Research Bulletin
Volume51
Issue number2
DOIs
StatePublished - Jan 15 2000
Externally publishedYes

Fingerprint

Pressoreceptors
Baroreflex
Neurons
Inbred SHR Rats
Arterial Pressure
Hypertension

Keywords

  • A1 area
  • Baroreceptor
  • Hypertension
  • Spontaneously hypertensive rats
  • Sympathoinhibition

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Baroreflex dependent and independent roles of the caudal ventrolateral medulla in cardiovascular regulation. / Sved, Alan F.; Ito, Satoru; Madden, Christopher (Chris).

In: Brain Research Bulletin, Vol. 51, No. 2, 15.01.2000, p. 129-133.

Research output: Contribution to journalArticle

@article{2630005930554d7fbaf80de406984396,
title = "Baroreflex dependent and independent roles of the caudal ventrolateral medulla in cardiovascular regulation",
abstract = "The caudal ventrolateral medulla (CVLM) plays a critical role in cardiovascular regulation. Convincing data now support the hypothesis that inhibition of sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) by CVLM neurons constitutes the necessary inhibitory link in baroreceptor reflex mediated control of sympathetic vasomotor outflow. Inhibition or destruction of the CVLM produces severe acute hypertension, consistent with blockade of baroreceptor reflexes and withdrawal of inhibition of RVLM sympathoexcitatory neurons. However, other data indicate that the CVLM also tonically inhibits RVLM sympathoexcitatory neurons in a manner not driven by baroreceptor input. In some studies, inhibition of the CVLM results in an increase in arterial pressure (AP) without inhibiting baroreceptor reflexes, possibly reflecting baroreceptor-independent and baroreceptor-dependent sub-regions of the CVLM. Furthermore, in baroreceptor- denervated rats, inhibition of the CVLM still leads to large increases in AP. In addition, in spontaneously hypertensive rats (SHR) central processing of baroreceptor reflexes appears normal but CVLM-mediated inhibition of the RVLM seems to be attenuated, suggesting that it is specifically a baroreceptor- independent mechanism of cardiovascular regulation in SHR that is altered. Taken together, these findings support an important, tonic, baroreceptor- independent inhibition of RVLM sympathoexcitatory neurons exerted by the CVLM. (C) 2000 Elsevier Science Inc.",
keywords = "A1 area, Baroreceptor, Hypertension, Spontaneously hypertensive rats, Sympathoinhibition",
author = "Sved, {Alan F.} and Satoru Ito and Madden, {Christopher (Chris)}",
year = "2000",
month = "1",
day = "15",
doi = "10.1016/S0361-9230(99)00234-8",
language = "English (US)",
volume = "51",
pages = "129--133",
journal = "Brain Research Bulletin",
issn = "0361-9230",
publisher = "Elsevier Inc.",
number = "2",

}

TY - JOUR

T1 - Baroreflex dependent and independent roles of the caudal ventrolateral medulla in cardiovascular regulation

AU - Sved, Alan F.

AU - Ito, Satoru

AU - Madden, Christopher (Chris)

PY - 2000/1/15

Y1 - 2000/1/15

N2 - The caudal ventrolateral medulla (CVLM) plays a critical role in cardiovascular regulation. Convincing data now support the hypothesis that inhibition of sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) by CVLM neurons constitutes the necessary inhibitory link in baroreceptor reflex mediated control of sympathetic vasomotor outflow. Inhibition or destruction of the CVLM produces severe acute hypertension, consistent with blockade of baroreceptor reflexes and withdrawal of inhibition of RVLM sympathoexcitatory neurons. However, other data indicate that the CVLM also tonically inhibits RVLM sympathoexcitatory neurons in a manner not driven by baroreceptor input. In some studies, inhibition of the CVLM results in an increase in arterial pressure (AP) without inhibiting baroreceptor reflexes, possibly reflecting baroreceptor-independent and baroreceptor-dependent sub-regions of the CVLM. Furthermore, in baroreceptor- denervated rats, inhibition of the CVLM still leads to large increases in AP. In addition, in spontaneously hypertensive rats (SHR) central processing of baroreceptor reflexes appears normal but CVLM-mediated inhibition of the RVLM seems to be attenuated, suggesting that it is specifically a baroreceptor- independent mechanism of cardiovascular regulation in SHR that is altered. Taken together, these findings support an important, tonic, baroreceptor- independent inhibition of RVLM sympathoexcitatory neurons exerted by the CVLM. (C) 2000 Elsevier Science Inc.

AB - The caudal ventrolateral medulla (CVLM) plays a critical role in cardiovascular regulation. Convincing data now support the hypothesis that inhibition of sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) by CVLM neurons constitutes the necessary inhibitory link in baroreceptor reflex mediated control of sympathetic vasomotor outflow. Inhibition or destruction of the CVLM produces severe acute hypertension, consistent with blockade of baroreceptor reflexes and withdrawal of inhibition of RVLM sympathoexcitatory neurons. However, other data indicate that the CVLM also tonically inhibits RVLM sympathoexcitatory neurons in a manner not driven by baroreceptor input. In some studies, inhibition of the CVLM results in an increase in arterial pressure (AP) without inhibiting baroreceptor reflexes, possibly reflecting baroreceptor-independent and baroreceptor-dependent sub-regions of the CVLM. Furthermore, in baroreceptor- denervated rats, inhibition of the CVLM still leads to large increases in AP. In addition, in spontaneously hypertensive rats (SHR) central processing of baroreceptor reflexes appears normal but CVLM-mediated inhibition of the RVLM seems to be attenuated, suggesting that it is specifically a baroreceptor- independent mechanism of cardiovascular regulation in SHR that is altered. Taken together, these findings support an important, tonic, baroreceptor- independent inhibition of RVLM sympathoexcitatory neurons exerted by the CVLM. (C) 2000 Elsevier Science Inc.

KW - A1 area

KW - Baroreceptor

KW - Hypertension

KW - Spontaneously hypertensive rats

KW - Sympathoinhibition

UR - http://www.scopus.com/inward/record.url?scp=0033972921&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033972921&partnerID=8YFLogxK

U2 - 10.1016/S0361-9230(99)00234-8

DO - 10.1016/S0361-9230(99)00234-8

M3 - Article

VL - 51

SP - 129

EP - 133

JO - Brain Research Bulletin

JF - Brain Research Bulletin

SN - 0361-9230

IS - 2

ER -