dc.description.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. | en |