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Hypertension, sodium retention, calcium excretion and osteopenia in Dahl rats. | LitMetric

AI Article Synopsis

  • DSS rats show abnormal calcium handling and bone disease linked to salt-sensitive hypertension.
  • During high salt intake, DSS rats initially retain calcium but later increase both sodium and calcium excretion.
  • This study suggests that sodium retention in DSS rats may be a compensatory response to maintain calcium balance amidst the challenges of chronic sodium loading.

Article 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.

Conclusion: 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.

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Source
http://dx.doi.org/10.1097/00004872-200404000-00024DOI Listing

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