Choice of Diuretic Therapy and Reconsideration for Aldosterone Receptors Blockers
2009; Lippincott Williams & Wilkins; Volume: 55; Issue: 1 Linguagem: Inglês
10.1161/hypertensionaha.109.147074
ISSN1524-4563
AutoresDecio Armanini, Cristina Fiore,
Tópico(s)Renin-Angiotensin System Studies
ResumoHomeHypertensionVol. 55, No. 1Choice of Diuretic Therapy and Reconsideration for Aldosterone Receptors Blockers Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBChoice of Diuretic Therapy and Reconsideration for Aldosterone Receptors Blockers Decio Armanini and Cristina Fiore Decio ArmaniniDecio Armanini Departments of Medical and Surgical Sciences-Endocrinology, University of Padua, Padua, Italy and Cristina FioreCristina Fiore Departments of Medical and Surgical Sciences-Endocrinology, University of Padua, Padua, Italy Originally published30 Nov 2009https://doi.org/10.1161/HYPERTENSIONAHA.109.147074Hypertension. 2010;55:e5Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: November 30, 2009: Previous Version 1 To the Editor:In an interesting editorial, Kaplan1 has focused recently on the choice of thiazide diuretics and concluded that chlorthalidone, alone or in addition to other antihypertensive drugs, may replace hydrochlorothiazide (HCTZ). The author also states that HCTZ and chlorthalidone, even at low doses (12.5 to 25.0 mg), can lower serum potassium and that an addition of small doses of spironolactone or eplerenone could provide maximal antihypertensive efficacy and prevent hypokalemia, particularly in resistant patients.A very important issue dealing with all diuretics is the volume depletion and activation of the renin-angiotensin-aldosterone system. Diuretics, with the exception of aldosterone receptor blockers, do not directly affect mineralocorticoid receptors. Recent studies of the literature have shown that aldosterone, even in situations of normal sodium intake, can enhance oxidative stress through activation of NADPH oxidase in particular clinical situations. Aldosterone is involved in inflammation atherosclerosis and heart hypertrophy and fibrosis, and the addition of aldosterone receptor blockers prevents the risk of complications in patients with heart diseases treated with other drugs (Randomized Aldactone Evaluation Study and Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study).Concerning the secondary hyperaldosteronism from diuretics, Brown and colleagues2,3 have compared the effect of HCTZ (25 mg per day) with the effect of spironolactone on the fibrinolytic balance in hypertensive subjects. Although HCTZ and spironolactone increased angiotensin II and aldosterone, only HCTZ increased plasminogen activator inhibitor 1 antigen concentration. Mineralocorticoid receptor antagonism prevents the effect of activation of the renin-angiotensin-aldosterone system on the plasminogen activator inhibitor 1 antigen in normotensive subjects and improves the fibrinolytic balance in hypertensive subjects through a potassium-independent mechanism, the same pro-oxidative effect that is evident when administering triamterene, thus supporting the concept that aldosterone increases plasminogen activator inhibitor 1 synthesis independently from the potassium concentration.2,3We have reported studies using human mononuclear leukocytes and have found that canrenone completely blocks the pro-oxidative effect of aldosterone in these cells, as measured by the protein expression of plasminogen activator inhibitor 1 and p22phox.4 In patients treated with thiazides or furosemide, aldosterone receptors are not blocked, and the cardiovascular risk is reduced by the lowering of blood pressure but is also enhanced by the binding of high aldosterone levels to mineralocorticoid receptors at the level of target tissues and, in particular, at the level of mononuclear leukocytes, a major component of vascular inflammation. This mechanism could enhance the fibrotic and atherogenic processes. These observations further enforce the concept that the goal of therapy is not only the lowering of blood pressure and the controlling of potassium but also the prevention of the inflammatory effect of aldosterone, as specified by Kaplan1 at the end of the editorial.Aldosterone receptor blockers do have a limited use in essential and secondary hypertension, particularly in Europe, as demonstrated by the Guidelines of the European Council of Hypertension (New Consensus Hypertension Guidelines from European Society of Hypertension/European Society of Cardiology 2007: Antihypertensive Treatment), which considers thiazides but not aldosterone receptors blockers for treatment of resistant hypertension, and maybe aldosterone receptor blockers should have a larger prescription, considering that metabolites with minimal (potassium canrenoate and canrenone) or absent (eplerenone) antiandrogenic activity are available in many countries.5DisclosuresNone.1 Kaplan NM. The choice of thiazide diuretics: why chlorthalidone may replace hydrochlorothiazide. Hypertension. 2009; 54: 951–953.LinkGoogle Scholar2 Sawathiparnich P, Kumar S, Vaughan DE, Brown NJ. Spironolactone abolishes the relationship between aldosterone and plasminogen activator inhibitor-1 in humans. J Clin Endocrinol Metab. 2002; 87: 448–452.CrossrefMedlineGoogle Scholar3 Ma J, Albornoz F, Yu Chang, Byrne DW, Vaughan DE, Brown NJ. Differing effects of mineralocorticoid receptor dependent and independent potassium-sparing diuretics on fibrinolytic balance. Hypertension. 2005; 46: 313–320.LinkGoogle Scholar4 Calò LA, Zaghetto F, Pagnin E, Davis PA, De Mozzi P, Sartorato P, Martire G, Fiore C, Armanini D. Effect of aldosterone and glycyrrhetinic acid on the protein expression of PAI-1 and p22(phox) in human mononuclear leukocytes. J Clin Endocrinol Metab. 2004; 89: 1973–1976.CrossrefMedlineGoogle Scholar5 Armanini D, Karbowiak I, Goi A, Mantero F, Funder JW. In-vivo metabolites of spironolactone and potassium canrenoate: determination of potential anti-androgenic activity by a mouse kidney cytosol receptor assay. Clin Endocrinol (Oxf). 1985; 23: 341–347.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Armanini D, Bordin L, Donà G, Andrisani A, Ambrosini G, Boscaro M and Sabbadin C (2019) Evaluation and implications of salt intake and excretion, The Journal of Clinical Hypertension, 10.1111/jch.13589, 21:7, (950-952), Online publication date: 1-Jul-2019. Armanini D, Sabbadin C, Andrisani A, Ambrosini G and Bordin L (2016) Some Considerations About Primary Aldosteronism and Its Follow-Up, The Journal of Clinical Hypertension, 10.1111/jch.12911, 18:12, (1213-1215), Online publication date: 1-Dec-2016. Grübler M, Kienreich K, Gaksch M, Verheyen N, Fahrleitner‐Pammer A, Schmid J, Grogorenz J, Ablasser K, Pieske B, Tomaschitz A and Pilz S (2014) Aldosterone to Active Renin Ratio Is Associated With Nocturnal Blood Pressure in Obese and Treated Hypertensive Patients: The Styrian Hypertension Study, The Journal of Clinical Hypertension, 10.1111/jch.12274, 16:4, (289-294), Online publication date: 1-Apr-2014. Fogari R, Derosa G, Zoppi A, Lazzari P, D'Angelo A and Mugellini A (2014) Comparative effect of canrenone or hydrochlorothiazide addition to valsartan/amlodipine combination on urinary albumin excretion in well-controlled type 2 diabetic hypertensive patients with microalbuminuria, Expert Opinion on Pharmacotherapy, 10.1517/14656566.2014.874415, 15:4, (453-459), Online publication date: 1-Mar-2014. January 2010Vol 55, Issue 1 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.109.147074PMID: 19948981 Originally publishedNovember 30, 2009 PDF download Advertisement SubjectsClinical Studies
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