4.4 Article

The association of plasma resistin with dietary sodium manipulation, the renin-angiotensin-aldosterone system, and 25-Hydroxyvitamin D3 in human hypertension

Journal

CLINICAL ENDOCRINOLOGY
Volume 74, Issue 3, Pages 294-299

Publisher

WILEY-BLACKWELL
DOI: 10.1111/j.1365-2265.2010.03922.x

Keywords

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Funding

  1. National Library of Medicine [F32 HL104776-01, F31 NR011108-01, K08 HL079929, KL2 RR025757, SDG 0735609T, K23 HL08236-03, U54LM008748]
  2. Harvard Clinical and Translational Science Center [UL1 RR025758]
  3. National Center for Research Resources
  4. National Institutes of Health, National Library of Medicine [F32 HL104776-01, F31 NR011108-01, K08 HL079929, KL2 RR025757, SDG 0735609T, K23 HL08236-03, U54LM008748]
  5. Harvard Clinical and Translational Science Center, from the National Center for Research Resources [UL1 RR025758]
  6. Brigham & Women's Hospital, General Clinical Research Center, from the National Center for Research Resources [M01-RR02635]
  7. Specialized Center of Research in Molecular Genetics of Hypertension [P50HL055000]

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P>Objective Both resistin and vitamin D have been associated with the renin-angiotensin-aldosterone system (RAAS). We investigated the association between resistin and the RAAS, and resistin and vitamin D under controlled dietary sodium conditions. Design Retrospective cross-sectional study of subjects from the HyperPATH Consortium, who were maintained in high dietary sodium (HS) and low dietary sodium (LS) balance for 1 week each. Patients Caucasian subjects with hypertension (n = 177). Measurements 25-hydroxyvitamin D (25[OH]D) levels were used to assess vitamin D status. Plasma resistin and RAAS measures were evaluated on each dietary intervention. Results Resistin levels were significantly higher in LS, where RAAS activity was high, when compared with HS balance, where RAAS activity was suppressed (6 center dot 36 vs 5 center dot 86 mu g/l, P < 0 center dot 0001); however, resistin concentrations were not associated with plasma renin activity or serum aldosterone on either diet. 25(OH)D levels were positively and independently associated with resistin in both dietary conditions (HS: beta = 0 center dot 400, P-trend = 0 center dot 027; LS: beta = 0 center dot 540, P-trend = 0 center dot 014). Conclusions Dietary sodium loading reduced resistin levels, possibly by suppressing the RAAS; however, circulating RAAS components were not related to resistin concentrations within each specific dietary sodium condition. 25(OH)D was positively associated with resistin and may be involved in resistin regulation through an unknown mechanism. Further studies to understand resistin regulation in human hypertension better are warranted.

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