The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study
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2006
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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.
Кључне речи:
temperature / heart rate / V-1a / V-1b / V-2 antagonistИзвор:
American Journal of Physiology - Regulatory Integrative & Comparative Physiology, 2006, 291, 6, R1579-R1591Издавач:
- Amer Physiological Soc, Bethesda
DOI: 10.1152/ajpregu.00764.2005
ISSN: 0363-6119
PubMed: 17085750
WoS: 000241768400002
Scopus: 2-s2.0-33845403130
Колекције
Институција/група
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 . .