The aim of this study was to generate hemorrhage-triggered fluctuations in blood pressure (BP) at low frequency (LF, < 0.2 Hz) in conscious rats and investigate with spectral analysis the relative roles of hemorrhage-activated catecholamines, the renin-angiotensin system (RAS), and arginine vasopressin (AVP) on the generation of these fluctuations. The individual contribution of these factors was assessed using a combination of the selective antagonists, prazosin, losartan, and Manning compound (AVPX). At rest, systolic BP (SBP) LF fluctuations were slightly increased by losartan. The mid-frequency (MF; 0.2-0.6 Hz) oscillations of SBP and diastolic BP (DBP) were decreased by prazosin alone or associated with AVPX or losartan. The high-frequency (HF; respiratory) oscillations of SBP were increased by prazosin, prazosin plus losartan, and prazosin plus AVPX. After severe hemorrhage (20 ml/kg), the spontaneous BP recovery was characterized by the occurrence of slow fluctuations of SBP and DBP, centered approximately 0.065 Hz, and by increases of MF (89%) oscillations of SBP. The HF component of SBP variability tended to be increased by blood loss. The occurrence of the SBP LF fluctuations was prevented when alpha 1-adrenergic activity was blocked by prazosin. These oscillations were always present, despite inhibition of angiotensin II, and were increased after inhibition of the AVP activity. Pretreatment with the specific inhibitors used in these studies favored the amplifying effect of hemorrhage on HF fluctuations while they prevented the postbleeding increase in MF oscillations. In conclusion, the present results show an association between the dependence of the postbleeding blood pressure level on catecholamines and the occurrence of slow fluctuations of BP. The buffering role of AVP suggests the establishment of a hierarchy between humoral systems in the genesis of the LF oscillations of BP, with the slow oscillations being generated by the main pressor system and being dampened by the other systems. The postbleeding rise in the MF component of SBP variability could be considered a reflection of the activations of both the sympathetic vasomotor drive and the RAS. The postbleeding increase in the HF component of BP variability was dampened by the activation of the humoral systems. These effects may reflect the low preload state due to hypovolemia.