Using a spectral procedure, we studied the effects of two treatment regimens of bradykinin (BK) on the blood pressure (BP) and heart rate (HR) variabilities in conscious Wistar rats. We performed a second series of experiments with hydralazine, at doses equihypotensive to those used in BK treatments, to discriminate between a specific effect of the peptide and those induced by vasodilation. We assessed the activity of the sympathetic nervous system (SNS), using the responses to atenolol and prazosin. First, at a subhypotensive treatment regimen, BK (5 micrograms/min) increased low-frequency (LF, 0.02-0.2 Hz) and mid-frequency (MF, 0.2-0.6 Hz) frequency components of BP variability and also activated the SNS. Lesser enhancements of LF and MF areas were induced by hydralazine (0.15 mg/kg). Second, high-dose treatment regimens of BK (100 micrograms/min) and hydralazine (2 mg/kg), which markedly decreased BP, did not change the areas of the LF and MF components of BP variability, whereas overactivity of the SNS was still assessed with the adrenergic blockers. On the other hand, high-dose BK induced a sixfold increase in the amplitude of the high frequency (HF, respiratory) component of BP. The effect of bradykinin on HF domain was associated with an increase in the depth of respiration in a group of anesthetized rats. Hoe 140 (60 micrograms/kg), a B-2 BK-receptor antagonist, abolished both the effects of BK on HF fluctuations in BP and the effects on breathing pattern. Our results demonstrate that BK induced different effects on LF and MF fluctuations in BP depending on the treatment regimen, whereas the SNS was activated by the two selected treatment regimens. Therefore, the MF component of BP variability should be considered only as a marker of the activity of the SNS when the BP level was not affected. Furthermore, we characterized an amplifying effect of BK on the HF domain of BP variability partly mediated by an increase in the depth of respiration.