Submitted on October 31, 2005
Accepted on July 20, 2006
The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study
Sanja Milutinovic1, David Murphy2, and Nina Japundzic Zigon1*
1 Institute of Pharmacology, Clinical Pharmacology and Toxicology, University of Belgrade School of Medicine, Belgrade, Serbia, Serbia And Montenegro
2 Neuroendocrinology Research Group, Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Bristol, United Kingdom; Institute of Pharmacology, Clinical Pharmacology and Toxicology, University of Belgrade School of Medicine, Belgrade, Serbia, Yugoslavia
* To whom correspondence should be addressed. E-mail: zigon{at}rcub.bg.ac.yu.
Whilst 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 V1a, V1b 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 20Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low frequency (LF-BP) and high frequency (HF-BP) domains. The effect of VP antagonists and of exogenous VP on body temperature (Tb), was also investigated . Under basal conditions, V1a antagonist increased HF-BP and Tb and this was prevented by metamizol. V1b antagonist enhanced HF-BP without affecting Tb and V2 antagonist increased VLF-BP variability which could be prevented by quinapril. Immobilization increased BP, LF-BP, HF-BP and HF-HR variability. V1a antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V1b antagonist prevented BP but not HR variability changes while V2 antagonist had no effect. Exogenous VP increased systolic arterial pressure (SAP) and HF-SAP variability and this was prevented by V1a and V1b, but not V2 antagonist pre-treatment. Our results suggest that, under basal conditions, VP, by stimulation of V1a, V1b and cognate V2 receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous VP, by stimulation of V1aor V1b, but not V2 receptors, increases BP variability revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively.
