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

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 MethodsResultsIn a double-blind placebo-controlled trial, we included 81 otherwise healthy postmenopausal women with high PTH levels (>6.9pmol/L) and vitamin D insufficiency (25(OH)D<50nmol/L). Participants received 2weeks of treatment with valsartan 80mg/d, vitamin D3 70g/d, valsartan plus vitamin D3 or double placebo. 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. ConclusionsIndependently 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.