AJP - Renal Information on EB 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Am J Physiol Renal Physiol (October 8, 2008). doi:10.1152/ajprenal.00531.2007
This Article
Right arrow Full Text (PDF)
Right arrow Supplemental Material
Right arrow All Versions of this Article:
295/6/F1752    most recent
00531.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Web of Science (2)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ziomber, A.
Right arrow Articles by Titze, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ziomber, A.
Right arrow Articles by Titze, J.
Submitted on November 12, 2007
Accepted on September 29, 2008

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

Agata Ziomber1, Agnes Machnik1, Anke Dahlmann1, Peter Dietsch2, Franz-Xaver Beck, Hubertus Wagner3, Karl F. Hilgers1, Friedrich C. Luft4, Kai-Uwe Eckardt1, and Jens Titze1*

1 Nephrology and Hypertension, Friedrich-Alexander-University Erlangen/Nurnberg, Germany
2 Biochemistry, Charite, Campus Benjamin Franklin, Berlin, Germany
3 Chemistry, Federal Centre for Nutrition and Food, Kulmbach, Germany
4 Franz Volhard Clinic, Humboldt University Berlin, Wiltbergstrasse 50, Berlin, 13125, Germany; , Germany

* To whom correspondence should be addressed. E-mail: jens.titze{at}rzmail.uni-erlangen.de.

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, Groups 3, 4, and 5 were DOCA-treated and received 1% NaCl, 1.44% NaHCO3, or 1.7% KHCO3 to drink. We measured mean arterial blood pressure (MAP) after 3 weeks directly. Tissue electrolyte and water content was measured by chemical analysis. Compared to controls, 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 total body (Na++K+) and water mass balance. Skin volume retention was hypertonic compared to serum and paralleled hypertension in DOCA-NaCl rats. These rats had higher TB(Na++K+)/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.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1977 by the American Physiological Society.