title: Acute genetic ablation of pendrin lowers blood pressure in mice.
abstract: BACKGROUND
  Pendrin, the chloride/bicarbonate exchanger of β-intercalated cells of the renal connecting tubule and the collecting duct, plays a key role in NaCl reabsorption by the distal nephron. Therefore, pendrin may be important for the control of extracellular fluid volume and blood pressure.
  
  
  METHODS
  Here, we have used a genetic mouse model in which the expression of pendrin can be switched-on in vivo by the administration of doxycycline. Pendrin can also be rapidly removed when doxycycline administration is discontinued. Therefore, our genetic strategy allows us to test selectively the acute effects of loss of pendrin function.
  
  
  RESULTS
  We show that acute loss of pendrin leads to a significant decrease of blood pressure. In addition, acute ablation of pendrin did not alter significantly the acid-base status or blood K +  concentration.
  
  
  CONCLUSIONS
  By using a transgenic mouse model, avoiding off-target effects related to pharmacological compounds, this study suggests that pendrin could be a novel target to treat hypertension.
authors.affiliation: INSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
authors.forename: Francesco
authors.initials: F
authors.lastname: Trepiccione
authors.affiliation: INSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
authors.forename: Christelle
authors.initials: C
authors.lastname: Soukaseum
authors.affiliation: INSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.|Hôpital Européen Georges Pompidou, Département de Physiologie, Assistance Publique-Hopitaux de Paris, Paris, France.
authors.forename: Veronique
authors.initials: V
authors.lastname: Baudrie
authors.affiliation: INSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Kumai
authors.affiliation: CNRS ERL 8228, INSERM UMRS 1138, Université Pierre et Marie Curie, Centre de Recherche des Cordeliers, Paris, France.
authors.forename: Jacques
authors.initials: J
authors.lastname: Teulon
authors.affiliation: INSERM U973, MTi-Bioinformatics; University Paris Diderot, Paris, France.
authors.forename: Bruno
authors.initials: B
authors.lastname: Villoutreix
authors.affiliation: Service d'Explorations Fonctionnelles Rénales, Hôpital Felix Guyon, CHU de la Réunion, St Denis, Ile de la Réunion, France.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Cornière
authors.affiliation: Anatomy and Physiology Department, Kansas State University, Manhattan, KS, USA.
authors.forename: Philine
authors.initials: P
authors.lastname: Wangemann
authors.affiliation: Otolaryngology Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Griffith
authors.affiliation: Otolaryngology Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA.
authors.forename: Yoon
authors.initials: Y
authors.lastname: Byung Choi
authors.affiliation: INSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.
authors.forename: Juliette
authors.initials: J
authors.lastname: Hadchouel
authors.affiliation: INSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Paris, France.|Centre National de la Recherche Scientifique, Paris, France.
authors.forename: Regine
authors.initials: R
authors.lastname: Chambrey
authors.affiliation: Service d'Explorations Fonctionnelles Rénales, Hôpital Felix Guyon, CHU de la Réunion, St Denis, Ile de la Réunion, France.
authors.forename: Dominique
authors.initials: D
authors.lastname: Eladari
mesh_terms: D000818:Animals; D027321:Anion Transport Proteins / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D000076988:Sulfate Transporters
chemical_list: D027321:Anion Transport Proteins; C494849:Slc26a4 protein, mouse; D000076988:Sulfate Transporters
keywords: chloride; diuretics; hypertension; intercalated cells; pendrin