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• W2337497110 abstract "HomeCirculationVol. 133, No. 16Letter by Campbell Regarding Article, “Statin Use and Adrenal Aldosterone Production in Hypertensive and Diabetic Subjects” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessLetterPDF/EPUBLetter by Campbell Regarding Article, “Statin Use and Adrenal Aldosterone Production in Hypertensive and Diabetic Subjects” Duncan J. CampbellMBBS, PhD Duncan J. CampbellDuncan J. Campbell St. Vincent’s Institute of Medical Research, Fitzroy, Victoria, Australia Search for more papers by this author Originally published19 Apr 2016https://doi.org/10.1161/CIRCULATIONAHA.115.020779Circulation. 2016;133:e605To the Editor:Baudrand et al1 reported that statin use was associated with lower plasma aldosterone levels and urinary aldosterone excretion in nonrandomized studies of hypertensive and diabetic subjects, both in the basal state and during stimulation by angiotensin II infusion or by a low sodium diet. They also reported that 10 μmol/L statins, a concentration that far exceeds peak plasma statin concentrations in patients, reduced the aldosterone secretory response of rat zona glomerulosa cells to angiotensin II and to potassium stimulation in vitro, and proposed that statins might reduce plasma aldosterone levels and urinary aldosterone excretion by inhibiting aldosterone steroidogenesis. However, mechanisms other than a direct effect of statins on aldosterone steroidogenesis should be considered.Baudrand et al1 reported no effect of statins on plasma cortisol levels or urinary cortisol excretion, but they did not measure plasma adrenocorticotropic hormone (ACTH) levels or examine the effects of statin therapy on ACTH-stimulated cortisol secretion. In a within-patient, placebo-controlled study, Mol et al2 found that simvastatin reduced basal plasma cortisol levels and increased basal plasma ACTH levels, thereby demonstrating that the effect of statin therapy on plasma cortisol levels needs to be examined in relation to factors that regulate cortisol secretion, such as ACTH. The effect of statins on aldosterone secretion should be similarly examined in relation to known regulators of aldosterone secretion, such as the renin angiotensin system and potassium. Baudrand et al1 state that “the aldosterone-to-renin ratio was not different when analyzed by statin use on both high and low salt diet,” which suggests that the effect of statins on basal aldosterone levels was explained, at least in part, by lower plasma renin activity in statin users not receiving antihypertensive therapy. It would be of interest to know whether plasma potassium concentrations were different between statin users and nonusers in their study of hypertensive subjects not receiving antihypertensive therapy.An additional mechanism by which statins may reduce aldosterone synthesis is the reduction in plasma low-density lipoprotein concentrations by statin therapy. Kovanen et al3 showed that adrenocortical cells obtain cholesterol for steroid synthesis from receptor-mediated uptake of plasma low-density lipoproteins. Moreover, rat zona glomerulosa cells show depletion in cholesterol ester content when stimulated by potassium,4 and potassium-stimulated aldosterone production by rat zona glomerulosa cells is enhanced when they are incubated in the presence of low-density lipoproteins,5 indicating that cholesterol supply for steroidogenesis is rate limiting when aldosterone secretion is stimulated. Thus, statins may lower aldosterone secretion by reducing plasma low-density lipoprotein concentrations and reducing cholesterol supply for steroidogenesis. There are, therefore, several mechanisms by which statins could reduce aldosterone secretion other than by a direct effect on aldosterone steroidogenesis.Duncan J. Campbell, MBBS, PhDSt. Vincent’s Institute of Medical ResearchFitzroy, Victoria, AustraliaDisclosuresNone.References1. Baudrand R, Pojoga LH, Vaidya A, Garza AE, Vöhringer PA, Jeunemaitre X, Hopkins PN, Yao TM, Williams J, Adler GK, Williams GH. Statin use and adrenal aldosterone production in hypertensive and diabetic subjects.Circulation. 2015; 132:1825–1833. doi: 10.1161/CIRCULATIONAHA.115.016759.LinkGoogle Scholar2. Mol MJ, Stalenhoef AF, Stuyt PM, Hermus AR, Demacker PN, Van ‘T Laar A. Effects of inhibition of cholesterol synthesis by simvastatin on the production of adrenocortical steroid hormones and ACTH.Clin Endocrinol (Oxf). 1989; 31:679–689.Google Scholar3. Kovanen PT, Faust JR, Brown MS, Goldstein JL. Low density lipoprotein receptors in bovine adrenal cortex. I. Receptor-mediated uptake of low density lipoprotein and utilization of its cholesterol for steroid synthesis in cultured adrenocortical cells.Endocrinology. 1979; 104:599–609. doi: 10.1210/endo-104-3-599.Google Scholar4. Campbell DJ. Stimulation by potassium of cholesterol ester depletion of rat zona glomerulosa cells in vitro.J Steroid Biochem. 1982; 17:707–708.CrossrefMedlineGoogle Scholar5. Campbell DJ. Effect of rat plasma lipoproteins on aldosterone production by rat zona glomerulosa cells in vitro.J Steroid Biochem. 1982; 17:709–711.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails April 19, 2016Vol 133, Issue 16Article InformationMetrics Download: 56 © 2016 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.115.020779PMID: 27142612 Originally publishedApril 19, 2016 PDF download SubjectsClinical StudiesHypertension" @default.
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