title: Na+/H+ exchangers: physiology and link to hypertension and organ ischemia.
abstract: OBJECTIVE
  Na/H exchangers (NHEs) are ubiquitous proteins with a very wide array of physiological functions, and they are summarized in this paper in view of the most recent advances. Hypertension and organ ischemia are two disease states of paramount importance in which NHEs have been implicated. The involvement of NHEs in the pathophysiology of these disorders is incompletely understood. This paper reviews the principal findings and current hypotheses linking NHE dysfunction to hypertension and ischemia.
  
  
  RESULTS
  With the advent of large-scale sequencing projects and powerful in-silico analyses, we have come to know what is most likely the entire mammalian NHE gene family. Recent advances have detailed the roles of NHE proteins, exploring new functions such as anchoring, scaffolding and pH regulation of intracellular compartments. Studies of NHEs in disease models, even though not conclusive to date, have contributed new evidence on the interplay of ion transporters and the delicate ion balances that may become disrupted.
  
  
  CONCLUSIONS
  This paper provides the interested reader with a concise overview of NHE physiology, and aims to address the implication of NHEs in the pathophysiology of hypertension and organ ischemia in light of the most recent literature.
authors.affiliation: Charles and Jane Pak Center for Mineral Metabolism and Clinical Research and Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 77530, USA.
authors.forename: I Alexandru
authors.initials: IA
authors.lastname: Bobulescu
authors.forename: Francesca
authors.initials: F
authors.lastname: Di Sole
authors.forename: Orson W
authors.initials: OW
authors.lastname: Moe
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D007511:Ischemia / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000503:physiopathology; D051379:Mice; D008954:Models, Biological; D017202:Myocardial Ischemia / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D015427:Reperfusion Injury / Q000235:genetics / Q000503:physiopathology; D017923:Sodium-Hydrogen Exchangers / Q000235:genetics / Q000502:physiology*
chemical_list: D017923:Sodium-Hydrogen Exchangers