SMILE – Repository of the Faculty of Dental Medicine
University of Belgrade - Faculty of Dental Medicine
    • English
    • Српски
    • Српски (Serbia)
  • English 
    • English
    • Serbian (Cyrillic)
    • Serbian (Latin)
  • Login
View Item 
  •   SMILE
  • Stomatološki fakultet
  • Radovi istraživača
  • View Item
  •   SMILE
  • Stomatološki fakultet
  • Radovi istraživača
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

Central cholinergic modulation of blood pressure short-term variability

Authorized Users Only
2006
Authors
Milutinović-Smiljanić, Sanja
Murphy, David
Japundžić-Žigon, Nina
Article (Published version)
Metadata
Show full item record
Abstract
The role of neurally born acetylcholine in the central modulation of cardiovascular short-term variability was assessed using a pharmacological probe physostigmine, a cholinesterase inhibitor that can act centrally also. Experiments were performed in instrumented conscious rats. Equidistant sampling at 20 Hz of systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and heart rate (HR) allowed direct spectral analysis. Spectra were analysed in the whole, very-low frequency (VLF), low-frequency (LF) and high-frequency (HF) domains. Physostigmine, but not neostigmine, increased SAP, LF SAP and HF SAP variability while neostigmine, but not physostigmine, decreased HR without affecting HR variability. Atropine methyl nitrate prevented neostigmine-induced bradycardia and potentiated the effects of physostigmine on DAP, LF DAP and HF DAP variability. Atropine sulphate, hexamethonium, phentolamine and metoprolol inhibited physostigmine-induced increase of SAP and LF SAP. Pre-treat...ment of rats by quinapril prevented physostigmine-induced increase of SAP, but not of LF SAP, while the V-1a antagonist prevented the increase of HF SAP. The results suggest that central cholinergic neurons facilitate but do not create LF SAP and HF SAP variability. The effect of physostigmine on LF SAP seems to be mediated via central muscarinic sites and the peripheral sympathetic system, while non-muscarinic central sites and vasopressin pathways subserve the increase of HF SAP.

Keywords:
blood pressure / physostigmine / cholinergic / sympathetic / spectral analysis / vasopressin
Source:
Neuropharmacology, 2006, 50, 7, 874-883
Publisher:
  • Pergamon-Elsevier Science Ltd, Oxford
Funding / projects:
  • Wellcome TrustWellcome Trust

DOI: 10.1016/j.neuropharm.2005.12.009

ISSN: 0028-3908

PubMed: 16487550

WoS: 000238724700011

Scopus: 2-s2.0-33646679434
[ Google Scholar ]
15
11
URI
https://smile.stomf.bg.ac.rs/handle/123456789/1307
Collections
  • Radovi istraživača
Institution/Community
Stomatološki fakultet
TY  - JOUR
AU  - Milutinović-Smiljanić, Sanja
AU  - Murphy, David
AU  - Japundžić-Žigon, Nina
PY  - 2006
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1307
AB  - The role of neurally born acetylcholine in the central modulation of cardiovascular short-term variability was assessed using a pharmacological probe physostigmine, a cholinesterase inhibitor that can act centrally also. Experiments were performed in instrumented conscious rats. Equidistant sampling at 20 Hz of systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and heart rate (HR) allowed direct spectral analysis. Spectra were analysed in the whole, very-low frequency (VLF), low-frequency (LF) and high-frequency (HF) domains. Physostigmine, but not neostigmine, increased SAP, LF SAP and HF SAP variability while neostigmine, but not physostigmine, decreased HR without affecting HR variability. Atropine methyl nitrate prevented neostigmine-induced bradycardia and potentiated the effects of physostigmine on DAP, LF DAP and HF DAP variability. Atropine sulphate, hexamethonium, phentolamine and metoprolol inhibited physostigmine-induced increase of SAP and LF SAP. Pre-treatment of rats by quinapril prevented physostigmine-induced increase of SAP, but not of LF SAP, while the V-1a antagonist prevented the increase of HF SAP. The results suggest that central cholinergic neurons facilitate but do not create LF SAP and HF SAP variability. The effect of physostigmine on LF SAP seems to be mediated via central muscarinic sites and the peripheral sympathetic system, while non-muscarinic central sites and vasopressin pathways subserve the increase of HF SAP.
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - Neuropharmacology
T1  - Central cholinergic modulation of blood pressure short-term variability
VL  - 50
IS  - 7
SP  - 874
EP  - 883
DO  - 10.1016/j.neuropharm.2005.12.009
ER  - 
@article{
author = "Milutinović-Smiljanić, Sanja and Murphy, David and Japundžić-Žigon, Nina",
year = "2006",
abstract = "The role of neurally born acetylcholine in the central modulation of cardiovascular short-term variability was assessed using a pharmacological probe physostigmine, a cholinesterase inhibitor that can act centrally also. Experiments were performed in instrumented conscious rats. Equidistant sampling at 20 Hz of systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and heart rate (HR) allowed direct spectral analysis. Spectra were analysed in the whole, very-low frequency (VLF), low-frequency (LF) and high-frequency (HF) domains. Physostigmine, but not neostigmine, increased SAP, LF SAP and HF SAP variability while neostigmine, but not physostigmine, decreased HR without affecting HR variability. Atropine methyl nitrate prevented neostigmine-induced bradycardia and potentiated the effects of physostigmine on DAP, LF DAP and HF DAP variability. Atropine sulphate, hexamethonium, phentolamine and metoprolol inhibited physostigmine-induced increase of SAP and LF SAP. Pre-treatment of rats by quinapril prevented physostigmine-induced increase of SAP, but not of LF SAP, while the V-1a antagonist prevented the increase of HF SAP. The results suggest that central cholinergic neurons facilitate but do not create LF SAP and HF SAP variability. The effect of physostigmine on LF SAP seems to be mediated via central muscarinic sites and the peripheral sympathetic system, while non-muscarinic central sites and vasopressin pathways subserve the increase of HF SAP.",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Neuropharmacology",
title = "Central cholinergic modulation of blood pressure short-term variability",
volume = "50",
number = "7",
pages = "874-883",
doi = "10.1016/j.neuropharm.2005.12.009"
}
Milutinović-Smiljanić, S., Murphy, D.,& Japundžić-Žigon, N.. (2006). Central cholinergic modulation of blood pressure short-term variability. in Neuropharmacology
Pergamon-Elsevier Science Ltd, Oxford., 50(7), 874-883.
https://doi.org/10.1016/j.neuropharm.2005.12.009
Milutinović-Smiljanić S, Murphy D, Japundžić-Žigon N. Central cholinergic modulation of blood pressure short-term variability. in Neuropharmacology. 2006;50(7):874-883.
doi:10.1016/j.neuropharm.2005.12.009 .
Milutinović-Smiljanić, Sanja, Murphy, David, Japundžić-Žigon, Nina, "Central cholinergic modulation of blood pressure short-term variability" in Neuropharmacology, 50, no. 7 (2006):874-883,
https://doi.org/10.1016/j.neuropharm.2005.12.009 . .

DSpace software copyright © 2002-2015  DuraSpace
About Smile – School of dental Medicine dIgitaL archivE | Send Feedback

OpenAIRERCUB
 

 

All of DSpaceCommunitiesAuthorsTitlesSubjectsThis institutionAuthorsTitlesSubjects

Statistics

View Usage Statistics

DSpace software copyright © 2002-2015  DuraSpace
About Smile – School of dental Medicine dIgitaL archivE | Send Feedback

OpenAIRERCUB