title: Acute reductions in blood flow restricted to the dorsomedial medulla induce a pressor response in rats.
abstract: OBJECTIVE
  The brainstem nucleus of the solitary tract (nucleus tractus solitarii, NTS) is a pivotal region for regulating the set-point of arterial pressure, the mechanisms of which are not fully understood. Based on evidence that the NTS exhibits O2-sensing mechanisms, we examined whether a localized disturbance of blood supply, resulting in hypoxia in the NTS, would lead to an acute increase in arterial pressure.
  
  
  METHODS
  Male Wistar rats were used. Cardiovascular parameters were measured before and after specific branches of superficial dorsal medullary veins were occluded; we assumed these were drainage vessels from the NTS and would produce stagnant hypoxia. Hypoxyprobe-1, a marker for detecting cellular hypoxia in the post-mortem tissue, was used to reveal whether vessel occlusion induced hypoxia within the NTS.
  
  
  RESULTS
  Following vessel occlusion, blood flow in the dorsal surface of the medulla oblongata including the NTS region showed an approximately 60% decrease and was associated with hypoxia in neurons located predominantly in the caudal part of the NTS as revealed using hypoxyprobe-1. Arterial pressure increased and this response was pronounced significantly in both magnitude and duration when baroreceptor reflex afferents were sectioned.
  
  
  CONCLUSIONS
  These results suggest that localized hypoxia in the NTS increases arterial pressure. We suggest this represents a protective mechanism whereby the elevated systemic pressure is a compensatory mechanism to enhance cerebral perfusion. Whether this physiological mechanism has any relevance to neurogenic hypertension is discussed.
authors.affiliation: Department of Physiology, Wakayama Medical University School of Medicine, Wakayama, Japan. h-waki@wakayama-med.ac.jp
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Waki
authors.forename: Mohammad E R
authors.initials: ME
authors.lastname: Bhuiyan
authors.forename: Sabine S
authors.initials: SS
authors.lastname: Gouraud
authors.forename: Miwa
authors.initials: M
authors.lastname: Takagishi
authors.forename: Atsutoshi
authors.initials: A
authors.lastname: Hatada
authors.forename: Akira
authors.initials: A
authors.lastname: Kohsaka
authors.forename: Julian F R
authors.initials: JF
authors.lastname: Paton
authors.forename: Masanobu
authors.initials: M
authors.lastname: Maeda
mesh_terms: D000818:Animals; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D002550:Cerebral Veins / Q000503:physiopathology; D004195:Disease Models, Animal; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000378:metabolism; D006973:Hypertension / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D008297:Male; D008526:Medulla Oblongata / Q000098:blood supply* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000502:physiology*; D017552:Solitary Nucleus / Q000098:blood supply* / Q000378:metabolism / Q000503:physiopathology
chemical_list: C497444:Hif1a protein, rat; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1; C105245:heme oxygenase-2