title: Hypertension, sodium retention, calcium excretion and osteopenia in Dahl rats.
abstract: BACKGROUND
  Salt-sensitive hypertension in the Dahl rat is associated with abnormalities in both calcium (Ca2+) and sodium (Na) homeostasis.
  
  
  OBJECTIVE
  To test the hypothesis that salt-induced abnormal Ca(2+) handling in Dahl salt-sensitive (DSS) rats is associated with negative Ca(2+) balance and bone disease.
  
  
  METHODS
  Ca(2+) excretion in acute and chronic Na(+) loading and electrolyte and water balance were determined by balance studies in Dahl salt-resistant (DSR) and salt-sensitive (DSS) rats fed 8 or 0.1% NaCl for 4 weeks. A dry ashing procedure was used to determine Na(+), Ca(2+), and water content and their association with blood pressure in the rats.
  
  
  RESULTS
  When fed 8% NaCl, DSS rats initially maintained a positive Ca(2+) balance and showed decreased natriuresis compared with DSR rats. During the course of Na(+) loading, DSS rats increased natriuresis and calciuresis. After 4 weeks of salt loading, cumulative Na balance was greater and cumulative Ca(2+) balance was less in DSS than in DSR rats. In addition, DSS rats developed osteopenia. Bone mineral content correlated inversely with blood pressure in DSS rats. Acute saline volume expansion in DSS rats demonstrated their ability to excrete the Na load fully, but led to an exaggerated renal loss of Ca(2+) compared with DSR rats.
  
  
  CONCLUSIONS
  DSS, but not DSR, develop Ca(2+) loss and ostopenia during chronic Na(+) loading. We speculate that Na retention in DSS rats fed a high Na diet may be in part a compensatory mechanism to maintain Ca(2+) balance.
authors.affiliation: Department of Medicine IV, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany. jus.titze@t-online.de
authors.forename: Jens
authors.initials: J
authors.lastname: Titze
authors.forename: Jörn
authors.initials: J
authors.lastname: Rittweger
authors.forename: Peter
authors.initials: P
authors.lastname: Dietsch
authors.forename: Holger
authors.initials: H
authors.lastname: Krause
authors.forename: Karl H
authors.initials: KH
authors.lastname: Schwind
authors.forename: Klaus
authors.initials: K
authors.lastname: Engelke
authors.forename: Rainer
authors.initials: R
authors.lastname: Lang
authors.forename: Karl A
authors.initials: KA
authors.lastname: Kirsch
authors.forename: Friedrich C
authors.initials: FC
authors.lastname: Luft
authors.forename: Karl F
authors.initials: KF
authors.lastname: Hilgers
mesh_terms: D000818:Animals; D001794:Blood Pressure; D015519:Bone Density; D001851:Bone Diseases, Metabolic / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism* / Q000652:urine; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D051381:Rats; D020303:Rats, Inbred Dahl; D012964:Sodium / Q000378:metabolism* / Q000652:urine; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage* / Q000378:metabolism; D013997:Time Factors; D014463:Ultrasonography; D014882:Water-Electrolyte Balance
chemical_list: D017673:Sodium Chloride, Dietary; D012964:Sodium; D002118:Calcium