SUMMARY The interplay of heart rate variability, baroreceptor control of heart rate, and blood pressure (BP) variability was examined in chronically instrumented, unanesthetized, freely moving rats in which the efferent neural influences on heart rate were pharmacologically altered. In each rat, BP was recorded continuously for 90 minutes in the control condition and in one or more of the following conditions: 1) /3-adrenergic receptor blockade by propranolol, 1 mg/kg; 2) cholinergic blockade by atropine, 0.75 mg/kg, and 3) combined blockade by propranolol plus atropine. Each BP recording was analyzed beat-to-beat by a computer that calculated heart rate and BP variabilities, both expressed as variation coefficients. In addition, under each condition the sensitivity of the arterial baroreceptor control of heart rate was assessed by measuring the reflex changes in pulse interval in response to BP changes induced by bolus i.v. injections of phenylephrine and nitroprusside. As compared with the control condition, 1) propranolol (n = 10) reduced heart rate variability by 23 ± 4% (p<0.01), only slightly impaired baroreceptor reflex sensitivity, and did not significantly modify BP variability ( +11 ± 7%); 2) atropine (n = 11) reduced heart rate variability by 30 ± 7% (p<0.01), drastically impaired baroreceptor reflex sensitivity, and increased BP variability ( + 40 ± 8 % , p<0.01); 3) combined blockade (n= 10) caused variability and baroreceptor reflex changes similar to those induced by atropine alone. Thus, heart rate variability depends on both vagal and sympathetic influences. However, only the former component affects BP variability, that is, it plays an antioscillatory role. This role is likely to originate from arterial baroreceptor modulation of vagal cardiac drive. (Hypertension 10: 533-537, 1987 Despite these considerations, our understanding of the mechanisms controlling BP variability is limited. Neurogenic influences are responsible for a substantial proportion of this phenomenon, 6 but it is unclear whether its overall magnitude depends more on central modulation of autonomic cardiovascular nerves than on the buffering action of arterial baroreceptor reflexes.7 A further open question concerns the relationship between BP variability and spontaneous heart rate variability, that is, whether heart rate variability plays no role in, enhances, or buffers the BP variations.In the present study pharmacological interventions interfering with the cardiac parasympathetic and sympathetic influences were used to examine the relationship of baroreceptor reflex sensitivity, heart rate variability, and BP variability. The study was conducted in unanesthetized, freely moving rats subjected to continuous BP and heart rate recordings to adequately assess the variability phenomena.