Effects of treatment with an angiotensin 2 receptor blocker and/or vitamin D3 on parathyroid hormone and aldosterone: A randomized, placebo‐controlled trial

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OBJECTIVE: Emerging evidence supports a positive, bidirectional and clinical relevant interaction between parathyroid hormone (PTH) and the renin-angiotensin-aldosterone-system (RAAS). A beneficial effect of the widely used RAAS inhibitors might include a PTH-lowering effect, as high PTH levels may be harmful to cardiovascular health. We aimed to investigate whether PTH levels are lowered by short-term treatment with an angiotensin 2 receptor blocker (valsartan) independently of coadministration of vitamin D3. Secondary end-points included effects on blood pressure, cardiac conduction and concentrations of renin and aldosterone. DESIGN AND METHODS: In a double-blind placebo-controlled trial, we included 81 otherwise healthy postmenopausal women with high PTH levels (>6.9 pmol/L) and vitamin D insufficiency (25(OH)D < 50 nmol/L). Participants received 2 weeks of treatment with valsartan 80 mg/d, vitamin D3 70 μg/d, valsartan plus vitamin D3 or double placebo. RESULTS: Valsartan treatment did not affect plasma PTH, although treatment reduced diastolic blood pressure (P = .01) and the aldosterone/renin ratio (P < .001). We found no associations between calciotropic hormones and RAAS markers. Vitamin D3 supplementation reduced PTH by 3.4% (25th, 75th -9.0 to 8.7) compared to a 7.1% increase (25th, 75th -2.4 to 30.9) in the placebo group (P = .01), but did not affect blood pressure, cardiac conduction or concentrations of renin and aldosterone. CONCLUSIONS: Independently of vitamin D3, short-term valsartan treatment did not reduce PTH. Vitamin D3 reduced PTH but did not affect blood pressure, cardiac conduction or the RAAS. The study does not support a direct association between PTH and aldosterone or a blood pressure-lowering effect of vitamin D3.

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