HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 291/6/R1579    most recent 00764.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Milutinovic, S. Articles by Japundzic-Zigon, N. Search for Related Content PubMed PubMed Citation Articles by Milutinovic, S. Articles by Japundzic-Zigon, N.

CALL FOR PAPERS
Neurohypophyseal Hormones: From Genomics and Physiology to Disease

The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study

Sanja Milutinovi,¹ David Murphy,^1,2 and Nina Japundi-igon¹

¹Institute of Pharmacology, Clinical Pharmacology and Toxicology School of Medicine University of Belgrade, Belgrade, Serbia; and ²The Molecular Neuroendocrinology Research Group, Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Bristol, United Kingdom

Submitted 31 October 2005 ; accepted in final form 20 July 2006

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 V₂ 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 V₂ 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 V₂ 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 V₂ antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V_1a, V_1b, and cognate V₂ receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous VP, by stimulation of V_1a or V_1b, but not V₂ receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively.

temperature; heart rate; V_1a; V_1b; V₂ antagonist