title: Internal sodium balance in DOCA-salt rats: a body composition study.
abstract: The idea that Na(+) retention inevitably leads to water retention is compelling; however, were Na(+) accumulation in part osmotically inactive, regulatory alternatives would be available. We speculated that in DOCA-salt rats Na(+) accumulation is excessive relative to water. Forty female Sprague-Dawley rats were divided into four subgroups. Groups 1 and 2 (controls) received tap water or 1% saline (salt) for 5 wk. Groups 3 and 4 received subcutaneous DOCA pellets and tap water or salt. Na(+), K(+), and water were measured in skin, bone, muscle, and total body by desiccation and consecutive dry ashing. DOCA-salt led to total body Na(+) excess (0.255 +/- 0.022 vs. 0.170 +/- 0.010 mmol/g dry wt; P < 0.001), whereas water retention was only moderate (0.685 +/- 0.119 vs. 0.648 +/- 0.130 ml/g wet wt; P < 0.001). Muscle Na(+) retention (0.220 +/- 0.029 vs. 0.145 +/- 0.021 mmol/g dry wt; P < 0.01) in DOCA-salt was compensated by muscle K(+) loss, indicating osmotically neutral Na(+)/K(+) exchange. Skin Na(+) retention (0.267 +/- 0.049 vs. 0.152 +/- 0.014 mmol/g dry wt; P < 0.001) in DOCA-salt rats was not balanced by K(+) loss, indicating osmotically inactive skin Na(+) storage. We conclude that DOCA-salt leads to tissue Na(+) excess relative to water. The relative Na(+) excess is achieved by two distinct mechanisms, namely, osmotically inactive Na(+) storage and osmotically neutral Na(+) retention balanced by K(+) loss. This "internal Na(+) escape" allows the maintenance of volume homeostasis despite increased total body Na(+).
authors.affiliation: Forschungslabor der Medizinischen Klinik IV, Kreuzburger Strasse 2, 90471 Nürnberg, Germany. jens.titze@rzmail.uni-erlangen.de
authors.forename: Jens
authors.initials: J
authors.lastname: Titze
authors.forename: Katharina
authors.initials: K
authors.lastname: Bauer
authors.forename: Markus
authors.initials: M
authors.lastname: Schafflhuber
authors.forename: Peter
authors.initials: P
authors.lastname: Dietsch
authors.forename: Rainer
authors.initials: R
authors.lastname: Lang
authors.forename: Karl H
authors.initials: KH
authors.lastname: Schwind
authors.forename: Friedrich C
authors.initials: FC
authors.lastname: Luft
authors.forename: Kai-Uwe
authors.initials: KU
authors.lastname: Eckardt
authors.forename: Karl F
authors.initials: KF
authors.lastname: Hilgers
mesh_terms: D000465:Algorithms; D000818:Animals; D001823:Body Composition / Q000187:drug effects*; D001835:Body Weight / Q000502:physiology; D003900:Desoxycorticosterone; D005260:Female; D006706:Homeostasis / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced* / Q000378:metabolism*; D008901:Mineralocorticoids / Q000378:metabolism; D009929:Organ Size / Q000502:physiology; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism / Q000652:urine; D051381:Rats; D020303:Rats, Inbred Dahl; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism* / Q000652:urine; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D008901:Mineralocorticoids; D003900:Desoxycorticosterone; D012964:Sodium; D011188:Potassium