ON THE ORIGIN OF LOW-FREQUENCY BLOOD-PRESSURE VARIABILITY IN THE CONSCIOUS DOG

1. Baroreceptor denervation increases blood pressure variability below 0.1 Hz. This study was undertaken to determine to what extent these f luctuations originate from the central nervous system or from cardiova scular sources. 2. Blood pressure was recorded at a rate of 10 Hz for similar to 3.5 h in conscious, resting dogs. Power density spectra wer e calculated from all 2(17) points of each recording session and integ rated between 0.0002 and 0.1 Hz. 3. Blockade of the afferent limb of t he baroreceptor reflex by surgical denervation of sinoaortic and cardi opulmonary afferents (Den; n = 6) significantly increased integrated p ower more than sixfold compared with a control group (n = 11). 4. Impa irment of the afferent limb in non-deafferented dogs by either alpha(1 )-adrenergic blockade with prazosin (Praz; n = 7) or ganglionic blocka de with hexamethonium (Hex; n = 6) Failed to raise variability. 5. Bot h prazosin (n = 6) and hexamethonium (n = 3) reduced the increased var iability in denervated dogs. 6. In non-deafferented dogs receiving hex amethonium, elevation of mean blood pressure to the hypertensive level of the Den group, by a continuous infusion of noradrenaline (n = 4), did not change the variability. 7. It is concluded that in the absence of chang es in posture, most of the increased blood pressure variabil ity after baroreceptor denervation is derived from the central nervous system. 8. Direct comparison of power spectra of the Den (total varia bility) and Hex groups (variability derived from the cardiovascular sy stem only) suggests that the central nervous system is also the preval ent source of low-frequency blood pressure variability in intact anima ls.