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      Statin Use and Adrenal Aldosterone Production in Hypertensive and Diabetic Subjects

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          Abstract

          Background

          Statins substantially reduce cardiovascular mortality and appear to have beneficial effects independent of their lipid lowering properties. We evaluated the hypothesis that statin use may modulate the secretion of aldosterone, a well-known contributor to cardiovascular disease.

          Methods and Results

          We measured adrenal hormones in two intervention studies. In study 1 in hypertensive subjects, aldosterone was analyzed at baseline and after angiotensin-II stimulation (AngII) on both high (HS) and low sodium (LS) diets (1122 observations, 15% on statins > 3 months). Statin users had 33% lower aldosterone levels in adjusted models (p < 0.001). Cortisol was not modified by statins. In secondary analyses, the lowest aldosterone levels were seen with lipophilic statins and with higher doses. Statin users had lower blood pressure (BP) and reduced salt sensitivity of BP (p=0.001). In study 2, aldosterone was measured in diabetic patients on a HS diet, before and after AngII stimulation (143 observations, 79% statin users). Again, statin users had 26% lower aldosterone levels (p =0.006), particularly those using lipophilic statins. Ex vivo studies in rat adrenal glomerulosa cells confirmed that lipophilic statins acutely inhibited aldosterone, but not corticosterone, in response to different secretagogues.

          Conclusions

          Statin use among hypertensive and diabetic subjects was associated with lower aldosterone secretion in response to AngII and LS diet in two human intervention studies. This effect appeared to be most pronounced with lipophilic statins and higher doses. Future studies to evaluate whether aldosterone inhibition may partially explain the robust cardioprotective effects of statins are warranted.

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          Author and article information

          Journal
          0147763
          2979
          Circulation
          Circulation
          Circulation
          0009-7322
          1524-4539
          25 September 2015
          02 October 2015
          10 November 2015
          10 November 2016
          : 132
          : 19
          : 1825-1833
          Affiliations
          [1 ]Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School. Boston, MA
          [2 ]Department of Endocrinology, School Of Medicine, Pontificia Universidad Catolica De Chile, Santiago, Chile
          [3 ]Hospital Clinico, Facultad Medicina Universidad de Chile, Santiago, Chile and Tufts Medical Center, Tufts University School of Medicine, Boston, MA
          [4 ]Centre Investigation Clinique, Hôpital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, Universite Paris Descartes, Paris, France
          [5 ]Cardiovascular Genetics Research, University of Utah School of Medicine Salt Lake City, UT
          Author notes
          Correspondence: Rene Baudrand, MD, Department of Endocrinology, School Of Medicine, Pontificia Universidad Catolica De Chile, Santiago 8330074, Chile, Phone/Fax: 562-2354-3095, rbaudran@ 123456uc.cl or Gordon H. Williams, MD, Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School. Boston, MA 02115, Phone: 617-525-7490, Fax: 617-582-6126, gwilliams@ 123456partners.org
          Article
          PMC4641753 PMC4641753 4641753 nihpa718657
          10.1161/CIRCULATIONAHA.115.016759
          4641753
          26432671
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