title: Arterial baroreflex inhibition by midbrain periaqueductal grey in anaesthetized rats.
abstract: Midbrain periaqueductal grey (PAG) provokes the defense reaction when stimulated. The present study was conducted to determine whether, and how, the PAG produces baroreflex inhibition, a feature characterizing the hypothalamic defense reaction. In chloralose-urethane anaesthetized rats, baroreflex vagal bradycardia and baroreflex hypotension were provoked by aortic depressor nerve stimulation. When the PAG was electrically stimulated baroreflex vagal bradycardia was remarkably suppressed; suppression of baroreflex hypotension was observed following bilateral vagotomy. In contrast, chemical stimulation of the PAG by D,L-homocysteic acid microinjection markedly suppressed baroreflex vagal bradycardia but only minimally suppressed baroreflex hypotension. These findings suggest that whereas overall PAG stimulation inhibits not only cardiac but also vascular components of baroreflexes, inhibition of the latter component either depends largely on activation of passing fibers or requires recruitment of a larger number of PAG cell bodies. PAG inhibition of baroreflex vagal bradycardia was not affected following spinal cord transection at C1, indicating that the inhibition was exclusively central in origin and not due to peripheral, prejunctional inhibition of vagal acetylcholine release by increased cardiac sympathetic nerve activities. The PAG inhibition of baroreflexes was greatly attenuated following electrolytic as well as chemical destruction of the parabrachial region. On the other hand, when the PAG was extensively lesioned, baroreflex inhibition produced by hypothalamic defense area stimulation was markedly diminished. PAG excitation thus causes powerful inhibition of arterial baroreflexes which is mediated by the parabrachial region; the PAG also mediates a major fraction of hypothalamic inhibition of the baroreflexes.
authors.affiliation: Department of Physiology, Mie University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Nosaka
authors.forename: K
authors.initials: K
authors.lastname: Murata
authors.forename: K
authors.initials: K
authors.lastname: Inui
authors.forename: S
authors.initials: S
authors.lastname: Murase
mesh_terms: D000758:Anesthesia; D000818:Animals; D001011:Aorta / Q000294:innervation; D001158:Arteries / Q000502:physiology*; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002346:Carotid Sinus / Q000502:physiology; D004558:Electric Stimulation; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006710:Homocysteine / Q000031:analogs & derivatives / Q000494:pharmacology; D007031:Hypothalamus / Q000502:physiology; D008297:Male; D008474:Medial Forebrain Bundle / Q000502:physiology; D008636:Mesencephalon / Q000502:physiology*; D010487:Periaqueductal Gray / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology
chemical_list: D006710:Homocysteine; C007956:homocysteic acid