Dynamic regulation of arterial blood pressure from the brainstem

Maintaining a static value of arterial pressure within a normal range is vital. On the other hand, evidence has demonstrated that proper arterial pressure variability (APV) is also im portant for normal health. Nowadays, power spectral analysis of arterial pressure for quantifying APV has gained in popularity. Using this tool, investigators has been able to evaluate various physiological mechanisms underlying APV. They have found three major spectral components of APV below the frequency of the heart rate. The high-frequency component is synchronized with respiratory rhythm, whereas the low-frequency (LF) and very low-frequency (VLF) components have been related to vasomotor activities. During cardiopulmonary bypass, while the heart is disconnected from the blood vessels, the VLF component still persists. In critical care units, the sustained disappearance of LF/VLF components for more than 2 days is a warning sign of impending mortality. Animal studies have revealed that pentobarbital anesthesia significantly suppresses the LF/VLF components in the rat. Antagonism of the α-adrenoceptor also suppresses these components. LF/VLF components are strongly exaggerated in spontaneously hypertensive rats (SHR) as compared to normotensive rats. Exploring the origins of LF/VLF components is also promising. These components occur in vegetative patients but not in brain-dead patients. Broad-band electrical stimulation of the rostral ventrolateral medulla (RVLM) largely induces LF/VLF components. These effects, however, are prevented by pretreatment with an α1-adrenoceptor antagonist. Apart from RVLM, many brain nuclei may also produce similar effects but with different physical characteristics. Frequency-modulated electroacupuncture on the Renzhong point significantly evoked LF/VLF components of APV. In addition, the dynamic regulation of arterial pressure from the RVLM in SHR is more potent and faster than that in normotensive rats. The above evidence strongly suggests that the LF/VLF components of APV originate from the brain stem, and are related to sympathetic activity, in which the α-adrenoceptor may play a major role. Enhancement of brainstem vasomotor control in SHR may partly explain their etiology of hypertension.