Sleep states alter ventral medullary surface responses to blood pressure challenges

Am J Physiol Regul Integr Comp Physiol. 2000 Apr;278(4):R1090-8. doi: 10.1152/ajpregu.2000.278.4.R1090.

Abstract

Ventral medullary surface (VMS) activity declines during rapid eye movement (REM) sleep, suggesting a potential for reduced VMS responsiveness to blood pressure challenges during that state. We measured VMS neural activity, assessed as changes in reflected 660-nm wavelength light, during pressor and depressor challenges within sleep/waking states in five adult, unrestrained, unanesthetized cats and in two control cats. Phenylephrine elevated blood pressure and elicited an initial VMS activity decline and a subsequent rise in VMS activity in all states, although the initial decline during quiet sleep occurred only in rostral placements. Phasic REM periods elicited a momentary recovery from the evoked activity rise, and arousals diminished the overall elevation in activity. A sodium nitroprusside depressor challenge increased VMS activity more in REM sleep than in quiet sleep, with the increase being even less in waking. Enhanced responses to depressor challenges during REM sleep suggest a loss of dampening of evoked activity during that state; state-related differential baroreflex sensitivity may result from sleep-waking changes in VMS responses to blood pressure challenges.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adrenergic alpha-Agonists / pharmacology
  • Anesthesia
  • Animals
  • Arousal / physiology
  • Baroreflex / physiology*
  • Blood Pressure / drug effects
  • Blood Pressure / physiology*
  • Cats
  • Diaphragm / physiology
  • Electrodes, Implanted
  • Electroencephalography
  • Evoked Potentials / physiology
  • Heart Rate / drug effects
  • Heart Rate / physiology
  • Medulla Oblongata / blood supply*
  • Medulla Oblongata / physiology*
  • Nitroprusside / pharmacology
  • Optics and Photonics
  • Phenylephrine / pharmacology
  • Pressoreceptors / physiology
  • Sleep, REM / physiology*
  • Vasodilator Agents / pharmacology

Substances

  • Adrenergic alpha-Agonists
  • Vasodilator Agents
  • Nitroprusside
  • Phenylephrine