Increased dietary salt enhances sympathoexcitatory and sympathoinhibitory responses from the rostral ventrolateral medulla

Julye M. Adams, Christopher J. Madden, Alan F. Sved, Sean Stocker

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

Increased dietary salt exaggerates arterial blood pressure (ABP) responses evoked from the rostral ventrolateral medulla (RVLM). The present study determined whether these enhanced pressor responses were directly attributable to a greater increase in sympathetic nerve activity (SNA) and whether these enhanced responses were balanced by a greater responsiveness of RVLM neurons to inhibitory input. Male Sprague-Dawley rats were fed normal chow and given access to either water or a 1% NaCl solution for 14 days. Injection of l-glutamate (0.03, 0.1, 1.0, and 3.0 nmol) into the RVLM produced a significantly greater increase in renal SNA, splanchnic SNA, and ABP in rats drinking 1% NaCl versus water. Conversely, injection of the inhibitory amino acid γ-aminobutyric acid (0.1, 1.0, and 10 nmol) into the RVLM produced significantly greater decreases in renal SNA, splanchnic SNA, and ABP of rats drinking 1% NaCl versus water. These enhanced SNA and ABP responses to l-glutamate and γ-aminobutyric acid were not observed in rats drinking 1% NaCl for 1 or 7 days but were present in rats drinking 1% NaCl for 21 days. Moreover, the dietary salt-induced enhancement of both sympathoexcitatory and sympathoinhibitory responses from the RVLM persisted after the 1% NaCl solution was replaced with water for 1, but not 7, days. These findings indicate that the potentiated ABP responses observed previously are mediated by parallel changes in SNA, and these responses depend on a slowly developing and reversible form of neuronal plasticity.

Original languageEnglish (US)
Pages (from-to)354-359
Number of pages6
JournalHypertension
Volume50
Issue number2
DOIs
StatePublished - Aug 1 2007

Fingerprint

Arterial Pressure
Salts
Drinking
Splanchnic Nerves
Aminobutyrates
Water
Glutamic Acid
Kidney
Injections
Neuronal Plasticity
Sprague Dawley Rats
Neurons
Amino Acids

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Adams, Julye M. ; Madden, Christopher J. ; Sved, Alan F. ; Stocker, Sean. / Increased dietary salt enhances sympathoexcitatory and sympathoinhibitory responses from the rostral ventrolateral medulla. In: Hypertension. 2007 ; Vol. 50, No. 2. pp. 354-359.
@article{4d4de1838e7b41be81432b17597d9ead,
title = "Increased dietary salt enhances sympathoexcitatory and sympathoinhibitory responses from the rostral ventrolateral medulla",
abstract = "Increased dietary salt exaggerates arterial blood pressure (ABP) responses evoked from the rostral ventrolateral medulla (RVLM). The present study determined whether these enhanced pressor responses were directly attributable to a greater increase in sympathetic nerve activity (SNA) and whether these enhanced responses were balanced by a greater responsiveness of RVLM neurons to inhibitory input. Male Sprague-Dawley rats were fed normal chow and given access to either water or a 1{\%} NaCl solution for 14 days. Injection of l-glutamate (0.03, 0.1, 1.0, and 3.0 nmol) into the RVLM produced a significantly greater increase in renal SNA, splanchnic SNA, and ABP in rats drinking 1{\%} NaCl versus water. Conversely, injection of the inhibitory amino acid γ-aminobutyric acid (0.1, 1.0, and 10 nmol) into the RVLM produced significantly greater decreases in renal SNA, splanchnic SNA, and ABP of rats drinking 1{\%} NaCl versus water. These enhanced SNA and ABP responses to l-glutamate and γ-aminobutyric acid were not observed in rats drinking 1{\%} NaCl for 1 or 7 days but were present in rats drinking 1{\%} NaCl for 21 days. Moreover, the dietary salt-induced enhancement of both sympathoexcitatory and sympathoinhibitory responses from the RVLM persisted after the 1{\%} NaCl solution was replaced with water for 1, but not 7, days. These findings indicate that the potentiated ABP responses observed previously are mediated by parallel changes in SNA, and these responses depend on a slowly developing and reversible form of neuronal plasticity.",
author = "Adams, {Julye M.} and Madden, {Christopher J.} and Sved, {Alan F.} and Sean Stocker",
year = "2007",
month = "8",
day = "1",
doi = "10.1161/HYPERTENSIONAHA.107.091843",
language = "English (US)",
volume = "50",
pages = "354--359",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

Increased dietary salt enhances sympathoexcitatory and sympathoinhibitory responses from the rostral ventrolateral medulla. / Adams, Julye M.; Madden, Christopher J.; Sved, Alan F.; Stocker, Sean.

In: Hypertension, Vol. 50, No. 2, 01.08.2007, p. 354-359.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Increased dietary salt enhances sympathoexcitatory and sympathoinhibitory responses from the rostral ventrolateral medulla

AU - Adams, Julye M.

AU - Madden, Christopher J.

AU - Sved, Alan F.

AU - Stocker, Sean

PY - 2007/8/1

Y1 - 2007/8/1

N2 - Increased dietary salt exaggerates arterial blood pressure (ABP) responses evoked from the rostral ventrolateral medulla (RVLM). The present study determined whether these enhanced pressor responses were directly attributable to a greater increase in sympathetic nerve activity (SNA) and whether these enhanced responses were balanced by a greater responsiveness of RVLM neurons to inhibitory input. Male Sprague-Dawley rats were fed normal chow and given access to either water or a 1% NaCl solution for 14 days. Injection of l-glutamate (0.03, 0.1, 1.0, and 3.0 nmol) into the RVLM produced a significantly greater increase in renal SNA, splanchnic SNA, and ABP in rats drinking 1% NaCl versus water. Conversely, injection of the inhibitory amino acid γ-aminobutyric acid (0.1, 1.0, and 10 nmol) into the RVLM produced significantly greater decreases in renal SNA, splanchnic SNA, and ABP of rats drinking 1% NaCl versus water. These enhanced SNA and ABP responses to l-glutamate and γ-aminobutyric acid were not observed in rats drinking 1% NaCl for 1 or 7 days but were present in rats drinking 1% NaCl for 21 days. Moreover, the dietary salt-induced enhancement of both sympathoexcitatory and sympathoinhibitory responses from the RVLM persisted after the 1% NaCl solution was replaced with water for 1, but not 7, days. These findings indicate that the potentiated ABP responses observed previously are mediated by parallel changes in SNA, and these responses depend on a slowly developing and reversible form of neuronal plasticity.

AB - Increased dietary salt exaggerates arterial blood pressure (ABP) responses evoked from the rostral ventrolateral medulla (RVLM). The present study determined whether these enhanced pressor responses were directly attributable to a greater increase in sympathetic nerve activity (SNA) and whether these enhanced responses were balanced by a greater responsiveness of RVLM neurons to inhibitory input. Male Sprague-Dawley rats were fed normal chow and given access to either water or a 1% NaCl solution for 14 days. Injection of l-glutamate (0.03, 0.1, 1.0, and 3.0 nmol) into the RVLM produced a significantly greater increase in renal SNA, splanchnic SNA, and ABP in rats drinking 1% NaCl versus water. Conversely, injection of the inhibitory amino acid γ-aminobutyric acid (0.1, 1.0, and 10 nmol) into the RVLM produced significantly greater decreases in renal SNA, splanchnic SNA, and ABP of rats drinking 1% NaCl versus water. These enhanced SNA and ABP responses to l-glutamate and γ-aminobutyric acid were not observed in rats drinking 1% NaCl for 1 or 7 days but were present in rats drinking 1% NaCl for 21 days. Moreover, the dietary salt-induced enhancement of both sympathoexcitatory and sympathoinhibitory responses from the RVLM persisted after the 1% NaCl solution was replaced with water for 1, but not 7, days. These findings indicate that the potentiated ABP responses observed previously are mediated by parallel changes in SNA, and these responses depend on a slowly developing and reversible form of neuronal plasticity.

UR - http://www.scopus.com/inward/record.url?scp=34547642988&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34547642988&partnerID=8YFLogxK

U2 - 10.1161/HYPERTENSIONAHA.107.091843

DO - 10.1161/HYPERTENSIONAHA.107.091843

M3 - Article

C2 - 17592069

AN - SCOPUS:34547642988

VL - 50

SP - 354

EP - 359

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 2

ER -