期刊
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
卷 97, 期 7, 页码 2456-2465出版社
ENDOCRINE SOC
DOI: 10.1210/jc.2012-1156
关键词
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资金
- American Medical Association Foundation Seed Grant
- National Library of Medicine [F32 HL104776-02, K23 HL111771-01, K23 HL08236-03, U54LM008748]
- Harvard Clinical and Translational Science Center [UL1 RR025758]
- National Center for Research Resources [UL1 RR025758, M01-RR02635]
- Brigham & Women's Hospital, General Clinical Research Center
- National Center for Research Resources
- Specialized Center of Research (SCOR) in Molecular Genetics of Hypertension [P50HL055000]
- Specialized Center of Research in Molecular Genetics of Hypertension [P50HL055000]
Context: Vitamin D deficiency and obesity are associated with increased tissue renin-angiotensin system (RAS) activity. Objective: The objective of the study was to evaluate whether vitamin D-3 therapy in obesity reduces tissue-RAS activity, as indicated by an increase in tissue sensitivity to angiotensin II (AngII). Participants: Participants included obese subjects with hypertension and 25-hydroxyvitamin D less than 25 ng/ml. Design: Subjects were studied before and after 1 month of vitamin D-3 15,000 IU/d, while in dietary sodium balance, and off all interfering medications. Fourteen subjects successfully completed all study procedures. Setting: The study was conducted at a clinical research center. Outcome Measures: At each study visit, tissue sensitivity to AngII was assessed by measuring renal plasma flow (RPF), mean arterial pressure (MAP), and adrenal secretion of aldosterone during an infusion of AngII. Subjects were then given captopril, and a second AngII infusion to evaluate the effect of captopril on tissue-RAS activity. Results: Vitamin D-3 therapy increased 25-hydroxyvitamin D (18 to 52 ng/ml) and basal RPF (+5%) and lowered supine MAP (-3%) (all P < 0.01). There was a greater decline in RPF and higher stimulation of aldosterone with AngII infusion after vitamin D-3 therapy (both P < 0.05). As anticipated, captopril increased the renal-vascular, MAP, and adrenal sensitivity to AngII, but this effect was much smaller after vitamin D-3 therapy, indicating that vitamin D-3 therapy corrected the tissue sensitivity to AngII akin to captopril. Conclusions: Vitamin D-3 therapy in obese hypertensives modified RPF, MAP, and tissue sensitivity to AngII similar to converting enzyme inhibition. Whether chronic vitamin D-3 therapy abrogates the development of diseases associated with excess RAS activity warrants investigation. (J Clin Endocrinol Metab 97: 2456-2465, 2012)
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