title: Brain stem NOS and ROS in neural mechanisms of hypertension.
abstract: CONCLUSIONS
  There is now compelling evidence to substantiate the notion that by depressing baroreflex regulation of blood pressure and augmenting central sympathetic outflow through their actions on the nucleus tractus solitarii (NTS) and rostral ventrolateral medulla (RVLM), brain stem nitric oxide synthase (NOS) and reactive oxygen species (ROS) are important contributing factors to neural mechanisms of hypertension. This review summarizes our contemporary views on the impact of NOS and ROS in the NTS and RVLM on neurogenic hypertension, and presents potential antihypertensive strategies that target brain stem NOS/ROS signaling.
  
  
  BACKGROUND
  NO signaling in the brain stem may be pro- or antihypertensive depending on the NOS isoform that generates this gaseous moiety and the site of action. Elevation of the ROS level when its production overbalances its degradation in the NTS and RVLM underlies neurogenic hypertension. Interventional strategies with emphases on alleviating the adverse actions of these molecules on blood pressure regulation have been investigated.
  
  
  RESULTS
  The pathological roles of NOS in the RVLM and NTS in neural mechanisms of hypertension are highly complex. Likewise, multiple signaling pathways underlie the deleterious roles of brain-stem ROS in neurogenic hypertension. There are recent indications that interactions between brain stem ROS and NOS may play a contributory role.
  
  
  CONCLUSIONS
  Given the complicity of action mechanisms of brain-stem NOS and ROS in neural mechanisms of hypertension, additional studies are needed to identify the most crucial therapeutic target that is applicable not only in animal models but also in patients suffering from neurogenic hypertension.
authors: Center for Translational Research in Biomedical Sciences, Kaohsiung Chang Gung Memorial Hospital , Kaohsiung, Taiwan, Republic of China .
authors: Samuel H H
authors: SH
authors: Chan
authors: Julie Y H
authors: JY
authors: Chan
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D001933:Brain Stem / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000209:etiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D000959:Antihypertensive Agents; D017382:Reactive Oxygen Species; D019001:Nitric Oxide Synthase