Hyperaldosteronism Medication

  • Author: George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London); Chief Editor: Stephen Kemp, MD, PhD   more...
 
Updated: May 10, 2012
 

Medication Summary

Aldosterone antagonists are indicated for the treatment of hyperaldosteronism. Hypokalemia and hypertension are also addressed with medications as needed.

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Aldosterone Antagonists, Selective

Class Summary

Aldosterone antagonists are used to lower the blood pressure, normalize serum potassium, and minimize postoperative hypoaldosteronism.

Spironolactone (Aldactone)

 

Spironolactone is the agent most commonly used to treat hyperaldosteronism because it directly antagonizes aldosterone effects at the distal tubule.

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Diuretics, Potassium-Sparing

Class Summary

Management of hypokalemia associated with hyperaldosteronism when spironolactone is contraindicated.

Triamterene (Dyrenium)

 

Triamterene inhibits reabsorption of sodium ions in exchange for potassium and hydrogen ions at the segment of the distal tubule that is under the control of adrenal mineralocorticoids (especially aldosterone). This activity is not directly related to aldosterone secretion or antagonism, and it is a result of a direct effect on the renal tubule.

The fraction of filtered sodium reaching this distal tubular exchange site is relatively small, and the amount that is exchanged depends on the level of mineralocorticoid activity; thus, the degree of natriuresis and diuresis produced by inhibition of the exchange mechanism is necessarily limited.

Increasing the amount of available sodium and the level of mineralocorticoid activity by using more proximally acting diuretics increases the degree of diuresis and potassium conservation. Triamterene may occasionally cause increases in serum potassium, which can result in hyperkalemia. It does not produce alkalosis, because it does not cause excessive excretion of titratable acid and ammonium.

Amiloride

 

Amiloride is an antikaliuretic drug with weak natriuretic, diuretic, and antihypertensive activity. It decreases the enhanced urinary excretion of magnesium that occurs when a thiazide or loop diuretic is used alone. It exerts a potassium-conserving effect in patients receiving kaliuretic diuretic agents.

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Antihypertensives, Other

Class Summary

Treatment of hypertension should be designed to lower blood pressure and reduce other risk factors of coronary heart disease. Pharmacologic therapy should be individualized on the basis of the patient’s age, race, known pathophysiologic variables, and concurrent conditions. Treatment should be aimed not only at lowering blood pressure safely and effectively but also at preventing or reversing hyperlipidemia, glucose intolerance, and left ventricular hypertrophy.

Nifedipine (Adalat, Procardia XL, Nifedical XL, Nifediac CC)

 

Nifedipine is a calcium channel blocker that produces vasodilation with antianginal and antihypertensive effects. It is available in both short-acting and sustained-release preparations.

Nifedipine acts by blocking postexcitation release of calcium ions into cardiac and vascular smooth muscle, thereby inhibiting the activation of adenosine triphosphatase (ATPase) on myofibril contraction. The overall effect is reduced intracellular calcium levels in cardiac and smooth muscle cells of the coronary and peripheral vasculature, resulting in dilatation of coronary and peripheral arteries.

Amlodipine (Norvasc)

 

Amlodipine is a calcium channel blocker that produces vasodilation with antianginal and antihypertensive effects. It acts by blocking the postexcitation release of calcium ions into cardiac and vascular smooth muscle, thereby inhibiting the activation of ATPase on myofibril contraction. The overall effect is reduced intracellular calcium levels in cardiac and smooth muscle cells of the coronary and peripheral vasculature, resulting in dilatation of coronary and peripheral arteries.

Diltiazem (Cardizem, Cardizem CD, Dilacor XR, Tiazac)

 

During depolarization, diltiazem inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It is a nondihydropyridine appropriate for prophylaxis of variant angina.

Nicardipine (Cardene)

 

Nicardipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption.

Verapamil (Calan, Calan SR, Covera HS, Isoptin, Verelan)

 

Verapamil is a nondihydropyridine that is appropriate for prophylaxis of variant angina. During depolarization, verapamil inhibits the entry of calcium ions into slow channels or voltage-sensitive areas of the vascular smooth muscle and myocardium.

Doxazosin (Cardura, Cardura XL)

 

Doxazosin is an alpha1-adrenergic antagonist, which causes vasodilation of veins and arterioles. These effects result in decreased peripheral resistance and blood pressure.

Prazosin (Minipress)

 

Prazosin is a postsynaptic alpha1-adrenergic antagonist. It causes vasodilation of veins and arterioles. These effects result in decreased peripheral resistance and blood pressure.

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Contributor Information and Disclosures
Author

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London)  Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

Antony Lafferty, MB ChB, FRACP  Senior Lecturer of Pediatric Endocrinology, Monash University Department of Pediatrics, National Institutes of Health, Bethesda, MD, and Princess Margaret Hospital for Children, Perth, Western Australia

Antony Lafferty, MB ChB, FRACP is a member of the following medical societies: Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Lynne Lipton Levitsky, MD Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor of Pediatrics, Harvard Medical School

Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Pfizer Grant/research funds P.I.; Tercica Grant/research funds Other; Eli Lily Grant/research funds PI; NovoNordisk Grant/research funds PI; NovoNordisk Consulting fee Consulting; Onyx Heart Valve Consulting fee Consulting

Thomas A Wilson, MD Professor of Clinical Pediatrics, Chief and Program Director, Division of Pediatric Endocrinology, Department of Pediatrics, The School of Medicine at Stony Brook University Medical Center

Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

References
  1. Funder JW. The genetic basis of primary aldosteronism. Curr Hypertens Rep. Apr 2012;14(2):120-4. [Medline].

  2. Escher G. Hyperaldosteronism in pregnancy. Ther Adv Cardiovasc Dis. Apr 2009;3(2):123-32. [Medline].

  3. Holland OB, Brown H, Kuhnert L, Fairchild C, Risk M, Gomez-Sanchez CE. Further evaluation of saline infusion for the diagnosis of primary aldosteronism. Hypertension. Sep-Oct 1984;6(5):717-23. [Medline].

  4. Ignatowska-Switalska H, Chodakowska J, Januszewicz W, Feltynowski T, Adamczyk M, Lewandowski J. Evaluation of plasma aldosterone to plasma renin activity ratio in patients with primary aldosteronism. J Hum Hypertens. Jun 1997;11(6):373-8. [Medline].

  5. Kasifoglu T, Akalin A, Cansu DU, Korkmaz C. Hypokalemic paralysis due to primary hyperaldosteronism simulating Gitelman's syndrome. Saudi J Kidney Dis Transpl. Mar 2009;20(2):285-7. [Medline].

  6. Künzel HE. Psychopathological symptoms in patients with primary hyperaldosteronism--possible pathways. Horm Metab Res. Mar 2012;44(3):202-7. [Medline].

  7. Schmiemann G, Gebhardt K, Hummers-Pradier E, Egidi G. Prevalence of hyperaldosteronism in primary care patients with resistant hypertension. J Am Board Fam Med. Jan-Feb 2012;25(1):98-103. [Medline].

  8. Gordon RD. Primary aldosteronism. J Endocrinol Invest. Jul-Aug 1995;18(7):495-511. [Medline].

  9. Gordon RD, Stowasser M, Klemm SA, Tunny TJ. Primary aldosteronism--some genetic, morphological, and biochemical aspects of subtypes. Steroids. Jan 1995;60(1):35-41. [Medline].

  10. Spence JD. Diagnosis of primary aldosteronism: for medical management, not just surgery. J Hypertens. Jan 2009;27(1):204-5; author reply 205. [Medline].

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Steroid biosynthetic pathway.
Physiologic regulation of the renin-angiotensin-aldosterone axis.
Table. Drugs Used in the Management of Idiopathic Hyperaldosteronism in Children
Drug Class Pediatric Dose
SpironolactoneAldosterone antagonist0-10 kg: 6.25 mg/dose PO q12h



11-20 kg: 12.5 mg/dose PO q12h



21-40 kg: 25 mg/dose PO q12h



>40 kg: 25 mg PO q8h



Potassium canrenoateAldosterone antagonist3-8 mg/kg IV qd; not to exceed 400 mg
AmiloridePotassium-sparing diuretic0.2 mg/kg q12h
TriamterenePotassium-sparing diuretic2 mg/kg/dose q8-24h
NifedipineDihydropyridine calcium channel antagonist0.25-0.5 mg/kg PO q6-8h
AmlodipineCalcium channel antagonist0.05-0.2 mg/ day PO
DoxazosinAlpha1 -specific adrenergic antagonist0.02-0.1 mg/day; not to exceed 4 mg
PrazosinAlpha1 -specific adrenergic antagonist0.005 mg/kg test dose, then 0.025-0.1 mg/kg/dose q6h; not to exceed 0.5 mg/dose
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