title: Sympatho-excitatory neurons of the rostral ventrolateral medulla are oxygen sensors and essential elements in the tonic and reflex control of the systemic and cerebral circulations.
abstract: MEDULLARY ROSTRAL VENTROLATERAL RETICULAR NUCLEUS (RVL): Reticulospinal neurons are critical to control of the circulation by the brain. Its actions are implemented by a few reticulospinal neurons, 200 in the rat. These directly innervate and excite preganglionic sympathetic neurons of the spinal cord by releasing L-glutamate. The RVL-spinal sympathetic premotor neurons are innervated by neurochemically diverse afferents from local and remote sources. They maintain arterial pressure tonically, mediate vasomotor reflexes elicited by stimulation of baro- or chemoreceptors or in response to pain or muscular exercise, and couple vasomotor responses to defense and conditioned fear behaviors. RVL-spinal neurons are central oxygen sensors, directly excited by hypoxia, and initiate sympathetic responses to cerebral ischemia or distortion (Cushing reflex). Stimulation of the RVL directly elevates cerebral flow independently of metabolism and initiates much of the cerebrovascular vasodilation in response to hypoxemia. RVL-SPINAL NEURONS IN RELATION TO HYPERTENSION AND SHOCK: RVL-spinal neurons are sites of action for many centrally acting antihypertensive drugs and some vasoactive hormones. Their integrity is required for expression of the elevated arterial pressure in neurogenic hypertension and for the compensatory sympathetic responses to hemorrhage. We propose that RVL-spinal neurons (1) maintain the activity of sympathetic neurons in mid-range amplifying, thereby, their signaling capacities; (2) initiate and integrate circulatory responses to a lack of oxygen so as to protect the brain from real or threatened hypoxia; (3) maintain, by tonic activity, normal expression of genes and gene products of central and peripheral sympathetic neurons and their peripheral targets that relate to their structure and neurotransmission-associated functions.
authors.affiliation: Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021, USA.
authors.forename: D J
authors.initials: DJ
authors.lastname: Reis
authors.forename: E V
authors.initials: EV
authors.lastname: Golanov
authors.forename: D A
authors.initials: DA
authors.lastname: Ruggiero
authors.forename: M K
authors.initials: MK
authors.lastname: Sun
mesh_terms: D000320:Adrenergic Fibers / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002628:Chemoreceptor Cells / Q000378:metabolism* / Q000503:physiopathology; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology; D008526:Medulla Oblongata / Q000166:cytology / Q000378:metabolism* / Q000503:physiopathology; D010100:Oxygen / Q000378:metabolism*; D011311:Pressoreceptors / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D010100:Oxygen