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Hypertension, sodium retention, calcium excretion and osteopenia in Dahl rats

Item Type:Article
Title:Hypertension, sodium retention, calcium excretion and osteopenia in Dahl rats
Creators Name:Titze, J. and Rittweger, J. and Dietsch, P. and Krause, H. and Schwind, K.H. and Engelke, K. and Lang, R. and Kirsch, K.A. and Luft, F.C. and Hilgers, K.F.
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 Ca2+ handling in Dahl salt-sensitive (DSS) rats is associated with negative Ca2+ balance and bone disease. Methods: Ca2+ 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+, Ca2+, and water content and their association with blood pressure in the rats. Results: When fed 8% NaCl, DSS rats initially maintained a positive Ca2+ 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 Ca2+ 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 Ca2+ compared with DSR rats. Conclusion: DSS, but not DSR, develop Ca2+ 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 Ca2+ balance.
Keywords:Hypertension, Sodium Retention, Calcium Excretion, Osteopenia, Dahl Rat, Animals, Rats
Source:Journal of Hypertension
Publisher:Lippincott Williams & Wilkins
Page Range:803-810
Date:April 2004
Official Publication:https://doi.org/10.1097/00004872-200404000-00024
PubMed:View item in PubMed

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