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Evidence for involvement of central vasopressin V1b and V2 receptors in stress-induced baroreflex desensitization

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2013
1829.pdf (764.8Kb)
Authors
Milutinović-Smiljanić, Sanja
Sarenac, Olivera
Lozic-Đurić, Maja
Murphy, David
Japundžić-Žigon, Nina
Article (Published version)
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Abstract
Background and Purpose It is well recognized that vasopressin modulates the neurogenic control of the circulation. Here, we report the central mechanisms by which vasopressin modulates cardiovascular response to stress induced by immobilization. Experimental Approach Experiments were performed in conscious male Wistar rats equipped with radiotelemetric device for continuous measurement of haemodynamic parameters: systolic and diastolic BP and heart rate (HR). The functioning of the spontaneous baro-receptor reflex (BRR) was evaluated using the sequence method and the following parameters were evaluated: BRR sensitivity (BRS) and BRR effectiveness index (BEI). Key Results Under baseline physiological conditions intracerebroventricular injection of 100 and 500ng of selective non-peptide V1a or V1b or V2 receptor antagonist did not modify BP, HR and BRR. Rats exposed to 15min long stress by immobilization exhibited increase of BP, HR, reduction of BRS and no change in BEI. Pretreatment of... rats with V1a receptor antagonist did not modulate the BP, HR, BRS and BEI response to stress. Pretreatment of rats with V1b receptor and V2 receptor antagonist, at both doses, prevented BRR desensitization and tachycardia, but failed to modulate stress-induced hypertension. Conclusions and Implications Vasopressin by the stimulation of central V1b- and V2-like receptors mediates stress-induced tachycardia and BRR desensitization. If these mechanisms are involved, BRR desensitization in heart failure and hypertension associated with poor outcome, they could be considered as novel targets for cardiovascular drug development.

Keywords:
V1a receptor antagonist / V1b receptor antagonist / V2 receptor antagonist / stress / baro-receptor reflex
Source:
British Journal of Pharmacology, 2013, 169, 4, 900-908
Publisher:
  • Wiley-Blackwell, Hoboken
Funding / projects:
  • Hypothalamic and medullary functional genomics in stress-induced hypertension (RS-41013)
  • Physiological Society (UK)

DOI: 10.1111/bph.12161

ISSN: 0007-1188

PubMed: 23488898

WoS: 000319477200016

Scopus: 2-s2.0-84878292703
[ Google Scholar ]
10
8
URI
https://smile.stomf.bg.ac.rs/handle/123456789/1834
Collections
  • Radovi istraživača
Institution/Community
Stomatološki fakultet
TY  - JOUR
AU  - Milutinović-Smiljanić, Sanja
AU  - Sarenac, Olivera
AU  - Lozic-Đurić, Maja
AU  - Murphy, David
AU  - Japundžić-Žigon, Nina
PY  - 2013
UR  - https://smile.stomf.bg.ac.rs/handle/123456789/1834
AB  - Background and Purpose It is well recognized that vasopressin modulates the neurogenic control of the circulation. Here, we report the central mechanisms by which vasopressin modulates cardiovascular response to stress induced by immobilization. Experimental Approach Experiments were performed in conscious male Wistar rats equipped with radiotelemetric device for continuous measurement of haemodynamic parameters: systolic and diastolic BP and heart rate (HR). The functioning of the spontaneous baro-receptor reflex (BRR) was evaluated using the sequence method and the following parameters were evaluated: BRR sensitivity (BRS) and BRR effectiveness index (BEI). Key Results Under baseline physiological conditions intracerebroventricular injection of 100 and 500ng of selective non-peptide V1a or V1b or V2 receptor antagonist did not modify BP, HR and BRR. Rats exposed to 15min long stress by immobilization exhibited increase of BP, HR, reduction of BRS and no change in BEI. Pretreatment of rats with V1a receptor antagonist did not modulate the BP, HR, BRS and BEI response to stress. Pretreatment of rats with V1b receptor and V2 receptor antagonist, at both doses, prevented BRR desensitization and tachycardia, but failed to modulate stress-induced hypertension. Conclusions and Implications Vasopressin by the stimulation of central V1b- and V2-like receptors mediates stress-induced tachycardia and BRR desensitization. If these mechanisms are involved, BRR desensitization in heart failure and hypertension associated with poor outcome, they could be considered as novel targets for cardiovascular drug development.
PB  - Wiley-Blackwell, Hoboken
T2  - British Journal of Pharmacology
T1  - Evidence for involvement of central vasopressin V1b and V2 receptors in stress-induced baroreflex desensitization
VL  - 169
IS  - 4
SP  - 900
EP  - 908
DO  - 10.1111/bph.12161
ER  - 
@article{
author = "Milutinović-Smiljanić, Sanja and Sarenac, Olivera and Lozic-Đurić, Maja and Murphy, David and Japundžić-Žigon, Nina",
year = "2013",
abstract = "Background and Purpose It is well recognized that vasopressin modulates the neurogenic control of the circulation. Here, we report the central mechanisms by which vasopressin modulates cardiovascular response to stress induced by immobilization. Experimental Approach Experiments were performed in conscious male Wistar rats equipped with radiotelemetric device for continuous measurement of haemodynamic parameters: systolic and diastolic BP and heart rate (HR). The functioning of the spontaneous baro-receptor reflex (BRR) was evaluated using the sequence method and the following parameters were evaluated: BRR sensitivity (BRS) and BRR effectiveness index (BEI). Key Results Under baseline physiological conditions intracerebroventricular injection of 100 and 500ng of selective non-peptide V1a or V1b or V2 receptor antagonist did not modify BP, HR and BRR. Rats exposed to 15min long stress by immobilization exhibited increase of BP, HR, reduction of BRS and no change in BEI. Pretreatment of rats with V1a receptor antagonist did not modulate the BP, HR, BRS and BEI response to stress. Pretreatment of rats with V1b receptor and V2 receptor antagonist, at both doses, prevented BRR desensitization and tachycardia, but failed to modulate stress-induced hypertension. Conclusions and Implications Vasopressin by the stimulation of central V1b- and V2-like receptors mediates stress-induced tachycardia and BRR desensitization. If these mechanisms are involved, BRR desensitization in heart failure and hypertension associated with poor outcome, they could be considered as novel targets for cardiovascular drug development.",
publisher = "Wiley-Blackwell, Hoboken",
journal = "British Journal of Pharmacology",
title = "Evidence for involvement of central vasopressin V1b and V2 receptors in stress-induced baroreflex desensitization",
volume = "169",
number = "4",
pages = "900-908",
doi = "10.1111/bph.12161"
}
Milutinović-Smiljanić, S., Sarenac, O., Lozic-Đurić, M., Murphy, D.,& Japundžić-Žigon, N.. (2013). Evidence for involvement of central vasopressin V1b and V2 receptors in stress-induced baroreflex desensitization. in British Journal of Pharmacology
Wiley-Blackwell, Hoboken., 169(4), 900-908.
https://doi.org/10.1111/bph.12161
Milutinović-Smiljanić S, Sarenac O, Lozic-Đurić M, Murphy D, Japundžić-Žigon N. Evidence for involvement of central vasopressin V1b and V2 receptors in stress-induced baroreflex desensitization. in British Journal of Pharmacology. 2013;169(4):900-908.
doi:10.1111/bph.12161 .
Milutinović-Smiljanić, Sanja, Sarenac, Olivera, Lozic-Đurić, Maja, Murphy, David, Japundžić-Žigon, Nina, "Evidence for involvement of central vasopressin V1b and V2 receptors in stress-induced baroreflex desensitization" in British Journal of Pharmacology, 169, no. 4 (2013):900-908,
https://doi.org/10.1111/bph.12161 . .

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