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This Article Full Text Full Text (PDF) Supplemental Material All Versions of this Article: 295/6/F1752    most recent 00531.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Ziomber, A. Articles by Titze, J. Search for Related Content PubMed PubMed Citation Articles by Ziomber, A. Articles by Titze, J.

Sodium-, potassium-, chloride-, and bicarbonate-related effects on blood pressure and electrolyte homeostasis in deoxycorticosterone acetate-treated rats

¹Department of Nephrology and Hypertension and Nikolaus Fiebiger Center for Molecular Medicine, Friedrich Alexander University, Erlangen-Nürnberg; ²Institute of Biochemistry, Charité Campus Benjamin Franklin, Berlin; ³Department of Physiology, University of Munich, Munich; ⁴Department of Safety and Quality of Meat, Max Rubner Institute, Kulmbach; and ⁵Experimental and Clinical Research Centre, Medical Faculty of the Charité, Max Delbrück Center for Molecular Medicine, HELIOS Klinikum Berlin-Brandenburg, Berlin, Germany

Submitted 12 November 2007 ; accepted in final form 29 September 2008

Na⁺ loading without Cl^– fails to increase blood pressure in the DOCA model. We compared the changes in the total body (TB) effective Na⁺, K⁺, Cl^–, and water (TBW) content as well as in intracellular (ICV) or extracellular (ECV) volume in rats receiving DOCA-NaCl, DOCA-NaHCO₃, or DOCA-KHCO₃. We divided 42 male rats into 5 groups. Group 1 was untreated, group 2 received 1% NaCl, and groups 3, 4, and 5 were treated with DOCA and received 1% NaCl, 1.44% NaHCO₃, or 1.7% KHCO₃ to drink. We measured mean arterial blood pressure (MAP) directly after 3 wk. Tissue electrolyte and water content was measured by chemical analysis. Compared with control rats, DOCA-NaCl increased MAP while DOCA-NaHCO₃ and DOCA-KHCO₃ did not. DOCA-NaCl increased TBNa⁺ 26% but only moderately increased TBW. DOCA-NaHCO₃ led to similar TBNa⁺ excess, while TBW and ICV, but not ECV, were increased more than in DOCA-NaCl rats. DOCA-KHCO₃ did not affect TBNa⁺ or volume. At a given TB(Na⁺+K⁺) and TBW, MAP in DOCA-NaCl rats was higher than in control, DOCA-NaHCO₃, and DOCA-KHCO₃ rats, indicating that hypertension in DOCA-NaCl rats was not dependent on TB(Na⁺+K⁺) and water mass balance. Skin volume retention was hypertonic compared with serum and paralleled hypertension in DOCA-NaCl rats. These rats had higher TB(Na⁺+K⁺)-to-TBW ratio in accumulated fluid than DOCA-NaHCO₃ rats. DOCA-NaCl rats also had increased intracellular Cl^– concentrations in skeletal muscle. We conclude that excessive cellular electrolyte redistribution and/or intracellular Na⁺ or Cl^– accumulation may play an important role in the pathogenesis of salt-sensitive hypertension.

DOCA-salt; salt-induced hypertension; autoregulation; osmotically inactive sodium