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Oral Calcium Supplementation Ambulatory Blood Pressure and Relation to Changes in Intracellular Ions and Sodium–Hydrogen Exchange Maria I. Pikilidou1, Christina D. Befani2, Pantelis A. Sarafidis1, Peter M. Nilsson3, George G. Koliakos2, Ioannis M. Tziolas1, Kiriakos A. Kazakos1, John G. Yovos1 and Anastasios N. Lasaridis1 Background Calcium (Ca2+) supplementation has been shown paradoxically to reduce intracellular Ca2+ and induce vascular relaxation. The aim of the study was to assess 24-h blood pressure (BP) change after Ca2+ supplementation and to investigate its relation to changes in intracellular ions and the activity of the first isoform of sodium– hydrogen exchange (NHE-1) in subjects with hypertension and type 2 diabetes. Methods This parallel, randomized controlled, single-blinded trial, consisted of 31 patients with type 2 diabetes, and hypertension who were allocated to receive 1,500 mg of Ca2+ per day (n = 15) or no treatment (n = 16) for 8 weeks. Results In the Ca2+ group a decrease of 1.7 ± 2.7 mm Hg (mean ± SE) P = 0.52 for mean 24-h systolic BP (SBP) and 2.1 ± 1.5 mm Hg, P = 0.19 for
There is experimental and clinical evidence indicating that hypertension clusters with insulin resistance and noninsulin dependent diabetes mellitus.1 Associations of both with cellular calcium (Ca2+) overload have been investigated.2,3 In particular, some have suggested that high levels of intracellular Ca2+, are linked to impaired insulin sensitivity as well as vascular smooth muscle tone, peripheral vascular resistance and blood pressure (BP).4,5 Over the past years many clinical trials on the effect of Ca2+ supplementation on BP, have been published and most of them are summarized in four meta-analyses.6–9 Altogether, they demonstrate a small but consistent drop in BP. Mechanisms offered for the effect of Ca2+ supplementation on BP, include lowering of intracellular Ca2+, increased sodium excretion 11st Department of Internal Medicine, Aristotle University of Thessaloniki,
AHEPA Hospital, Thessaloniki, Greece; 2Department of Biological Chemistry, Medical School, Aristotle University, Thessaloniki, Greece; 3Department of Clinical Sciences, Malmö University Hospital, Lund University, Malmö, Sweden. Correspondence: Maria I. Pikilidou (
[email protected]) Received 28 March 2009; first decision 7 June 2009; accepted 24 August 2009; advance online publication 24 September 2009. doi:10.1038/ajh.2009.182 © 2009 American Journal of Hypertension, Ltd.
mean 24-h diastolic BP (DBP) was recorded. Whereas in the control group an increase of 1.4 ± 2.7 mm Hg, P = 0.59 for mean 24-h SBP and 1.2 ± 2.8 mm Hg, P = 0.83 for mean 24-h DBP was observed. Intraplatelet Ca2+ decreased whereas intraplatelet magnesium (Mg2+) and erythrocyte K+ increased in the intervention group. Change in mean 24-h SBP in the pooled group correlated with both change in intraplatelet Ca2+ (r = 0.49, P < 0.05) and NHE-1 activity (r = 0.6, P
