title: Late-developing rostral ventrolateral medullary surface responses to cardiovascular challenges during sleep.
abstract: Pressor and depressor manipulations are usually followed by compensatory autonomic, respiratory, somatomotor or arousal responses that limit the extent of blood pressure change. Of neural sites participating in blood pressure control, the rostral ventrolateral medullary surface (RVLMS) contributes significantly, and exhibits rapid-onset overall activity declines and increases to pressor and depressor challenges, respectively. In addition, longer-latency physiological responses develop that further compensate for the homeostatic challenge; some of these later influences are associated with arousal. Late-developing RVLMS activity changes accompanying physiologic responses that normalize a cardiovascular manipulation may provide insights into compensatory neural mechanisms during sleep following sustained or extreme blood pressure changes. We used intrinsic optical imaging procedures in seven unanesthetized adult cats to examine RVLMS and control site responses to pressor and depressor challenges during sleep that resulted in somatomotor, respiratory, heart rate or electroencephalographic indications of late-developing (post-baroreflex) compensatory responses. Although initial RVLMS responses differed in direction between pressor and depressor challenges, neural activity increased later in both manipulations, coincident with overt physiological manifestations indicative of compensatory responses, including arousal. Arousal occurred in 44% of blood pressure challenges. Comparable late-developing neural activity increases were not apparent in control sites. Latencies of late RVLMS responses during rapid eye movement sleep were significantly longer than in quiet sleep for pressor challenges. The pattern of the late RVLMS responses was not dependent on arousal, and suggests that the RVLMS participates in both the early baroreflex response and the late-developing compensatory actions.
authors.affiliation: Department of Neurobiology, UCLA School of Medicine, 10833 LeConte Avenue, Los Angeles, CA 90095-1763, USA.
authors.forename: Christopher A
authors.initials: CA
authors.lastname: Richard
authors.forename: David M
authors.initials: DM
authors.lastname: Rector
authors.forename: Paul M
authors.initials: PM
authors.lastname: Macey
authors.forename: Noorjahan
authors.initials: N
authors.lastname: Ali
authors.forename: Ronald M
authors.initials: RM
authors.lastname: Harper
mesh_terms: D000818:Animals; D001143:Arousal / Q000502:physiology; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000187:drug effects*; D002415:Cats; D004567:Electrodes, Implanted; D004569:Electroencephalography; D005071:Evoked Potentials / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects; D008526:Medulla Oblongata / Q000098:blood supply* / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D012119:Respiration / Q000187:drug effects; D012890:Sleep; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine