The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study
Abstract
Although it has been suggested that vasopressin (VP) acts within the central nervous system to modulate autonomic cardiovascular controls, the mechanisms involved are not understood. Using nonpeptide, selective V-1a, V-1b, and V-2 antagonists, in conscious rats, we assessed the roles of central VP receptors, under basal conditions, after the central application of exogenous VP, and after immobilization, on cardiovascular short-term variability. Equidistant sampling of blood pressure (BP) and heart rate (HR) at 20 Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low-frequency (LF-BP), and high-frequency (HF-BP) blood pressure domains. The effect of VP antagonists and of exogenous VP on body temperature (T-b) was also investigated. Under basal conditions, V-1a antagonist increased HF-BP and T-b, and this was prevented by metamizol. V-1b antagonist enhanced HF-BP without affecting T-b, and V-2 antagonist increased VLF-BP variability which could be prevented by quinapril.... Immobilization increased BP, LF-BP, HF-BP, and HF-HR variability. V-1a antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V-1b antagonist prevented BP but not HR variability changes, whereas V-2 antagonist had no effect. Exogenous VP increased systolic arterial pressure ( SAP) and HF-SAP variability, and this was prevented by V-1a and V-1b but not V-2 antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V-1a, V-1b, and cognate V-2 receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous V-P, by stimulation of V-1a or V-1b, but not V-2 receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively.
Keywords:
temperature / heart rate / V-1a / V-1b / V-2 antagonistSource:
American Journal of Physiology - Regulatory Integrative & Comparative Physiology, 2006, 291, 6, R1579-R1591Publisher:
- Amer Physiological Soc, Bethesda
DOI: 10.1152/ajpregu.00764.2005
ISSN: 0363-6119
PubMed: 17085750
WoS: 000241768400002
Scopus: 2-s2.0-33845403130
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Stomatološki fakultetTY - JOUR AU - Milutinović-Smiljanić, Sanja AU - Murphy, David AU - Japundžić-Žigon, Nina PY - 2006 UR - https://smile.stomf.bg.ac.rs/handle/123456789/1319 AB - Although it has been suggested that vasopressin (VP) acts within the central nervous system to modulate autonomic cardiovascular controls, the mechanisms involved are not understood. Using nonpeptide, selective V-1a, V-1b, and V-2 antagonists, in conscious rats, we assessed the roles of central VP receptors, under basal conditions, after the central application of exogenous VP, and after immobilization, on cardiovascular short-term variability. Equidistant sampling of blood pressure (BP) and heart rate (HR) at 20 Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low-frequency (LF-BP), and high-frequency (HF-BP) blood pressure domains. The effect of VP antagonists and of exogenous VP on body temperature (T-b) was also investigated. Under basal conditions, V-1a antagonist increased HF-BP and T-b, and this was prevented by metamizol. V-1b antagonist enhanced HF-BP without affecting T-b, and V-2 antagonist increased VLF-BP variability which could be prevented by quinapril. Immobilization increased BP, LF-BP, HF-BP, and HF-HR variability. V-1a antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V-1b antagonist prevented BP but not HR variability changes, whereas V-2 antagonist had no effect. Exogenous VP increased systolic arterial pressure ( SAP) and HF-SAP variability, and this was prevented by V-1a and V-1b but not V-2 antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V-1a, V-1b, and cognate V-2 receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous V-P, by stimulation of V-1a or V-1b, but not V-2 receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively. PB - Amer Physiological Soc, Bethesda T2 - American Journal of Physiology - Regulatory Integrative & Comparative Physiology T1 - The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study VL - 291 IS - 6 SP - R1579 EP - R1591 DO - 10.1152/ajpregu.00764.2005 ER -
@article{ author = "Milutinović-Smiljanić, Sanja and Murphy, David and Japundžić-Žigon, Nina", year = "2006", abstract = "Although it has been suggested that vasopressin (VP) acts within the central nervous system to modulate autonomic cardiovascular controls, the mechanisms involved are not understood. Using nonpeptide, selective V-1a, V-1b, and V-2 antagonists, in conscious rats, we assessed the roles of central VP receptors, under basal conditions, after the central application of exogenous VP, and after immobilization, on cardiovascular short-term variability. Equidistant sampling of blood pressure (BP) and heart rate (HR) at 20 Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low-frequency (LF-BP), and high-frequency (HF-BP) blood pressure domains. The effect of VP antagonists and of exogenous VP on body temperature (T-b) was also investigated. Under basal conditions, V-1a antagonist increased HF-BP and T-b, and this was prevented by metamizol. V-1b antagonist enhanced HF-BP without affecting T-b, and V-2 antagonist increased VLF-BP variability which could be prevented by quinapril. Immobilization increased BP, LF-BP, HF-BP, and HF-HR variability. V-1a antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V-1b antagonist prevented BP but not HR variability changes, whereas V-2 antagonist had no effect. Exogenous VP increased systolic arterial pressure ( SAP) and HF-SAP variability, and this was prevented by V-1a and V-1b but not V-2 antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V-1a, V-1b, and cognate V-2 receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous V-P, by stimulation of V-1a or V-1b, but not V-2 receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively.", publisher = "Amer Physiological Soc, Bethesda", journal = "American Journal of Physiology - Regulatory Integrative & Comparative Physiology", title = "The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study", volume = "291", number = "6", pages = "R1579-R1591", doi = "10.1152/ajpregu.00764.2005" }
Milutinović-Smiljanić, S., Murphy, D.,& Japundžić-Žigon, N.. (2006). The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study. in American Journal of Physiology - Regulatory Integrative & Comparative Physiology Amer Physiological Soc, Bethesda., 291(6), R1579-R1591. https://doi.org/10.1152/ajpregu.00764.2005
Milutinović-Smiljanić S, Murphy D, Japundžić-Žigon N. The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study. in American Journal of Physiology - Regulatory Integrative & Comparative Physiology. 2006;291(6):R1579-R1591. doi:10.1152/ajpregu.00764.2005 .
Milutinović-Smiljanić, Sanja, Murphy, David, Japundžić-Žigon, Nina, "The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study" in American Journal of Physiology - Regulatory Integrative & Comparative Physiology, 291, no. 6 (2006):R1579-R1591, https://doi.org/10.1152/ajpregu.00764.2005 . .