Primary Aldosteronism Medication
- Author: Gabriel I Uwaifo, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP more...
In nonsurgical primary aldosteronism, medical therapy is the treatment of choice. The drug that is the treatment of first choice for most variants of nonsurgical primary aldosteronism is spironolactone, which is used to achieve normoaldosteronism and to assist with blood pressure control. Potassium supplementation should not be routinely administered with spironolactone because of the potential for the development of hyperkalemia.
In patients who are unable to tolerate spironolactone, other potassium-sparing diuretics, such as amiloride and triamterene, can be used, although these are considered less ideal options.
Glucocorticoid-remediable aldosteronism (GRA) is treated with small doses of glucocorticosteroids (ie, hydrocortisone, prednisone). At optimal doses, glucocorticosteroids normalize aldosterone and blood pressure.
Various antihypertensives may be added to achieve adequate blood pressure control. The dihydropyridine calcium channel blockers (eg, nifedipine) directly inhibit aldosterone production; however, while producing significant improvement in patients with hypertension (HTN), they do not address pathophysiology. Plasma renin activity (PRA), aldosterone levels, plasma volume, and serum potassium concentrations remain essentially unchanged with nifedipine use.
Other second-step agents for blood pressure control include thiazide diuretics, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor blockers.
A sodium-restricted diet (< 80 mEq or < 2 g of sodium daily), maintenance of ideal body weight, and regular aerobic exercise contribute substantially to the success of pharmacologic treatment.
Aldosterone Antagonists, Selective
These agents compete with aldosterone receptor sites, reducing edema and ascites.
Spironolactone competitively binds receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. It provides diuretic and antihypertensive effects, causing increased excretion of sodium and water, while retaining potassium. Spironolactone is administered alone or with a diuretic agent that acts on the proximal renal tubule. Spironolactone may block the effects of aldosterone on arteriolar smooth muscles.
Eplerenone selectively blocks aldosterone at the mineralocorticoid receptors in epithelial (eg, kidney) and nonepithelial (eg, heart, blood vessels, brain) tissues, thus decreasing blood pressure and sodium reabsorption.
These agents are used as second-line medication for the treatment of primary aldosteronism due to nonlateralizing disease and/or lateralizing disease for which surgery is otherwise contraindicated or refused. They often must be used with other antihypertensives to achieve the best blood pressure control, because they are not potent antihypertensives.
Triamterene is a potassium-sparing diuretic with relatively weak natriuretic properties. It exerts a diuretic effect on the distal renal tubule to inhibit reabsorption of sodium in exchange for potassium and hydrogen. Triamterene increases sodium excretion and reduces the excessive loss of potassium and hydrogen associated with hydrochlorothiazide. It is not a competitive antagonist of mineralocorticoids; its potassium-conserving effect is observed in patients with Addison disease (ie, without aldosterone).
The onset and duration of activity with triamterene are similar to those of hydrochlorothiazide. No predictable antihypertensive effect is demonstrated. It is rapidly absorbed following oral administration, and peak plasma levels are achieved within 1 hour of dosing. Triamterene is primarily metabolized to a sulfate conjugate of hydroxytriamterene. Plasma and urine levels of this metabolite greatly exceed triamterene levels.
Amiloride is a pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. It is a potassium-conserving (antikaliuretic) drug that, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity. Amiloride's effects have been partially additive to the effects of thiazide diuretics in some clinical studies. When it is administered with a thiazide or loop diuretic, it has been shown to decrease the enhanced urinary excretion of magnesium that occurs when a thiazide or loop diuretic is used alone.
Amiloride has potassium-conserving activity in patients receiving kaliuretic-diuretic agents. Amiloride is not an aldosterone antagonist, and its effects are observed in the absence of aldosterone. It exerts its potassium-sparing effect through the inhibition of sodium reabsorption at the distal convoluted tubule, cortical collecting tubule, and collecting duct. This decreases the net negative potential of the tubular lumen and reduces potassium and hydrogen secretion and their subsequent excretions.
Amiloride usually begins to act within 2 hours after an oral dose. Its effect on electrolyte excretion reaches a peak between 6-10 hours and lasts about 24 hours. Peak plasma levels are obtained in 3-4 hours, and the drug's plasma half-life varies between 6 and 9 hours.
Amiloride is not metabolized by the liver; it is instead excreted unchanged by the kidneys. Within 72 hours, about 50% of a dose of amiloride is excreted in urine and 40% in stool. The drug has little effect on the glomerular filtration rate or on renal blood flow. Because the liver does not metabolize amiloride hydrochloride, drug accumulation is not anticipated in patients with hepatic dysfunction; however, accumulation can occur if hepatorenal syndrome develops.
Amiloride should rarely be used alone. Used as single agents, potassium-sparing diuretics, including amiloride, result in an increased risk of hyperkalemia (approximately 10% with amiloride). Amiloride should be used alone only when persistent hypokalemia has been documented and only with careful titration of the dose and close monitoring of serum electrolyte levels.
Thiazide diuretics inhibit the reabsorption of sodium in the distal tubules, increasing the excretion of sodium, water, and potassium and hydrogen ions. They have been effective in treating hypertension of various etiologies. Besides diminishing sodium reabsorption, they also appear to diminish the sensitivity of blood vessels to circulating vasopressor substances. In all patients treated with diuretics, electrolyte levels should be monitored. Examples of thiazide diuretics are hydrochlorothiazide and chlorthalidone.
Hydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as of potassium and hydrogen ions.
Chlorthalidone inhibits the reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as of potassium and hydrogen ions.
Calcium channel Blockers
Calcium channel blockers affect blood pressure by decreasing vascular peripheral resistance. With short-acting calcium channel blockers, the cardiac response to this action is variable and tachycardia can occur. Long-acting preparations may cause a decrease in heart rate.
Calcium channel blockers are classified by their structure and have different degrees of selectivity in their effects on vascular smooth muscle. The dihydropyridines do not exert electrophysiologic effects and are commonly used to manage hypertension. Facial flushing may occur. Examples of calcium channel blockers include amlodipine and isradipine.
Amlodipine is generally regarded as a dihydropyridine, although experimental evidence suggests that it also may bind to nondihydropyridine binding sites. It is appropriate for the prophylaxis of variant angina and has antianginal and antihypertensive effects. Amlodipine blocks the postexcitation release of calcium ions into cardiac and vascular smooth muscle, thereby inhibiting the action of adenosine triphosphatase (ATPase) on myofibril contraction.
The overall effect of amlodipine 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 also increases myocardial oxygen delivery in patients with vasospastic angina, and it may potentiate angiotensin-converting enzyme (ACE) inhibitor effects.
During depolarization, amlodipine inhibits the entrance of calcium ions into slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. It has a substantially longer half-life than nifedipine and diltiazem and is administered once daily.
Felodipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. It benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. It can be used during pregnancy if clinically indicated.
Calcium channel blockers potentiate ACE inhibitor effects. Renal protection is not proven, but these agents reduce morbidity and mortality rates in congestive heart failure. Calcium channel blockers are indicated in patients with diastolic dysfunction. They are effective as monotherapy in black patients and elderly patients.
Isradipine is a dihydropyridine calcium channel blocker. It inhibits the entrance of calcium into select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization. This causes relaxation of coronary vascular smooth muscle, which results in coronary vasodilation. Vasodilation reduces systemic resistance and blood pressure, with a small increase in resting heart rate. Isradipine also has negative inotropic effects.
Extended-release nifedipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery.
Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and lower aldosterone secretion. They are effective and well-tolerated drugs with no adverse effects on plasma lipid levels or glucose tolerance. They prevent the progression of diabetic nephropathy and other forms of glomerulopathies but appear to be less effective in black patients than in white patients. ACE inhibitors are contraindicated in pregnancy.
Patients with high plasma renin activity (PRA) may have an excessive hypotensive response to ACE inhibitors. Patients with bilateral renal vascular disease or with a single kidney, whose renal perfusion is maintained by high levels of angiotensin II, may develop irreversible acute renal failure when treated with ACE inhibitors, and caution should be exercised with their use in these patients. Interestingly, although primary aldosteronism is a condition associated with low plasma renin, aldosterone secretion seems to be exquisitely sensitive to even subnormal concentrations of angiotensin II. This phenomenon seems to be the basis for the efficacy of ACE inhibitors in primary aldosteronism (specifically idiopathic adrenal hyperplasia [IAH]).
Cough and angioedema are less common with newer members of this class than with captopril. Serum potassium and serum creatinine concentrations should be monitored for the development of hyperkalemia and azotemia. Agents in this class include captopril, lisinopril, and enalapril.
Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. It is rapidly absorbed, but bioavailability is significantly reduced with food intake. Captopril achieves a peak concentration in 1 hour and has a short half-life. The drug is cleared by the kidney; impaired renal function requires reduction of the dosage. Captopril is absorbed well orally.
Give captopril at least 1 hour before meals. If it is added to water, use it within 15 minutes. The dose can be low initially, then titrated upward as needed and as tolerated by the patient.
Enalapril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. The drug helps to control blood pressure and proteinuria. Enalapril decreases the pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance.
Enalapril has a favorable clinical effect when administered over a long period. Because it helps to prevent potassium loss in the distal tubules, enalapril reduces the amount of oral potassium supplementation needed by the patient.
Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Benazepril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
When pediatric patients are unable to swallow tablets or the calculated dose does not correspond with tablet strength, an extemporaneous suspension can be compounded. Combine 300 mg (15 tabs of 20 mg strength) in 75 mL of Ora-Plus suspending vehicle and shake well for at least 2 minutes. Let the tablets sit and dissolve for at least 1 hour, then shake again for 1 minute. Add 75 mL of Ora-Sweet. The final concentration is 2 mg/mL, with a total volume of 150 mL. The expiration time is 30 days with refrigeration.
Fosinopril is a competitive ACE inhibitor. It prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.
Quinapril is a competitive ACE inhibitor. It reduces angiotensin II levels, decreasing aldosterone secretion.
Ramipril inhibits partially inhibits both tissue and circulating ACE activity, therefore reducing the formation of angiotensin II in the tissue and plasma. Ramipril has an antihypertensive effect even in patients with low-renin hypertension.
Angiotensin II Receptor Blockers
Angiotensin II receptor blockers lower blood pressure by blocking the final receptor (ie, angiotensin II) in the renin-angiotensin axis. Like angiotensin-converting enzyme (ACE) inhibitors, they are contraindicated in pregnancy. Serum electrolyte and creatinine levels should be monitored. Irbesartan and losartan are examples of angiotensin II receptor blockers (ARBs). Interestingly, although primary aldosteronism is a condition associated with low plasma renin, aldosterone secretion seems to be exquisitely sensitive to even subnormal concentrations of angiotensin II. This phenomenon seems to be the basis for the efficacy of ARBs in primary aldosteronism (specifically idiopathic adrenal hyperplasia [IAH]).
Irbesartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II at the tissue receptor site. It may induce a more complete inhibition of the renin-angiotensin system than do ACE inhibitors. In addition, irbesartan does not affect the response to bradykinin, and it is less likely to be associated with cough and angioedema.
Losartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors do. In addition, losartan does not affect the response to bradykinin, and it is less likely to be associated with cough and angioedema. It is suitable for patients who are unable to tolerate ACE inhibitors.
Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to angiotensin II type 1 receptors in vascular smooth muscle. Its action is independent of the pathways for angiotensin II synthesis.
Valsartan is a prodrug that displaces angiotensin II from angiotensin II type 1 receptors, blocking the vasoconstrictor effects of angiotensin II. Valsartan may also lower blood pressure through its effects on aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses.
Valsartan may induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors do. In addition, it does not affect the response to bradykinin and is less likely to be associated with cough and angioedema. Valsartan is suitable for patients who are unable to tolerate ACE inhibitors.
Telmisartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland and therefore reduces blood pressure. There is also an AT2 receptor found in many tissues, but AT2 is not known to be associated with cardiovascular homeostasis and telmisartan has much greater affinity for the AT1 receptor than for the AT2 receptor
This class of agents are therapeutically appropriate only for the GRA subtype of primary aldosteronism. The treatment of choice in GRA is the administration of the lowest possible dose of glucocorticoid that can be used to achieve adequate blood pressure control. Because of the potential adverse effects that can result from even subtle glucocorticoid excess, using short-acting glucocorticoids, such as prednisone and hydrocortisone (rather than dexamethasone), is generally best.
Prednisone is a short-acting prodrug that exerts its effects after it undergoes metabolism and is converted to prednisolone. Prednisone mimics naturally occurring cortisol and is used in GRA to rapidly suppress aldosterone levels and resolve the volume expansion and hypertension in this disorder, being generally efficacious within 2 weeks of treatment initiation.
Hydrocortisone possesses a molecular similarity to aldosterone and therefore not only binds to the glucocorticoid receptor (thus resulting in resulting in lower aldosterone levels in GRA), but also the mineralocorticoid receptor (MR), thus also providing competitive inhibition of ambient aldosterone levels at the MR level (resulting in decreased physiologic effects of existing ambient aldosterone levels in GRA).
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