Aldosterone is a hormone produced by your adrenal glands that controls how much sodium and water your body holds onto, directly influencing your blood pressure and fluid balance. It belongs to a class of hormones called mineralocorticoids, and it’s synthesized in the outermost layer of the adrenal cortex, a region called the zona glomerulosa. Though it rarely gets the same attention as cortisol or adrenaline, aldosterone plays a central role in keeping your blood pressure stable, your electrolytes balanced, and your kidneys functioning properly.
How Aldosterone Works in the Body
Aldosterone’s primary job happens in the kidneys, specifically in the latter portion of the filtering tubes (called the distal tubules and collecting ducts). When aldosterone reaches these cells, it passes through the cell membrane and binds to a receptor inside the cell. That binding triggers the cell to produce more sodium channels and sodium-potassium pumps, essentially telling the kidney to pull sodium back into the bloodstream instead of letting it leave in urine.
When sodium gets reabsorbed, water follows it. This increases blood volume and raises blood pressure. At the same time, for every sodium molecule that gets pulled back in, potassium gets pushed out into the urine. This sodium-potassium exchange is the core of what aldosterone does: it raises sodium and lowers potassium. It also helps regulate acid levels in the blood by promoting the excretion of hydrogen ions.
This is why aldosterone problems tend to show up as blood pressure issues or abnormal potassium levels, often before anything else becomes noticeable.
What Triggers Aldosterone Release
Your body doesn’t release aldosterone randomly. It’s part of a tightly regulated chain reaction called the renin-angiotensin-aldosterone system, or RAAS. The process starts in the kidneys: specialized cells near the kidney’s filtering units detect drops in blood pressure, low sodium levels, or signals from the sympathetic nervous system. In response, they release an enzyme called renin, which kicks off a cascade that ultimately produces a molecule called angiotensin II. Angiotensin II then signals the adrenal glands to release aldosterone.
Rising potassium levels in the blood can also directly stimulate aldosterone release, independent of the renin pathway. This makes sense biologically: if potassium climbs too high, the heart and muscles can malfunction, so the body uses aldosterone to flush the excess out through the kidneys. Once blood pressure normalizes and potassium drops back to a safe range, the signals quiet down and aldosterone production tapers off.
What Happens When Aldosterone Is Too High
When the body produces too much aldosterone on its own, typically from a growth on one of the adrenal glands or from overactive tissue in both glands, the condition is called primary hyperaldosteronism (sometimes called Conn’s syndrome). The excess aldosterone causes the kidneys to retain too much sodium and water while dumping too much potassium, which drives blood pressure up persistently.
The hallmark sign is high blood pressure that resists treatment. A characteristic presentation is someone whose blood pressure stays elevated despite taking three or more blood pressure medications. Other symptoms stem from low potassium: fatigue, muscle weakness, headaches, excessive thirst, and frequent urination. Some people experience abdominal bloating or cramping. That said, many patients never develop obviously low potassium on blood tests, so the condition can go undetected for years if clinicians aren’t looking for it specifically.
Beyond the immediate symptoms, chronically elevated aldosterone causes damage that goes well beyond the kidneys. High aldosterone levels promote scarring (fibrosis) in heart muscle, stiffen blood vessels, and impair the inner lining of arteries. This increases the risk of heart attacks, strokes, and heart failure over time, making early detection important even when symptoms seem manageable.
What Happens When Aldosterone Is Too Low
Low aldosterone levels usually occur as part of a broader condition called adrenal insufficiency, where the adrenal glands can’t produce enough of several hormones at once. The most well-known form is Addison’s disease, which in developed countries is caused by autoimmune damage to the adrenal glands in roughly 8 or 9 out of every 10 cases. Tuberculosis, HIV-related infections, and certain medications can also destroy adrenal tissue.
Without enough aldosterone, the kidneys can’t retain sodium properly. Sodium and water are lost in urine, which causes low blood pressure, dehydration, and a buildup of potassium. Common symptoms include chronic fatigue, muscle weakness, weight loss, loss of appetite, nausea, and craving salty foods (which makes intuitive sense, since the body is losing salt). Blood pressure often drops further when standing up, causing dizziness or fainting. People with Addison’s disease may also develop darkened patches of skin on scars, skin folds, elbows, knees, and inside the cheeks.
How Aldosterone Levels Are Tested
The standard screening test for aldosterone problems is a blood draw that measures both aldosterone and renin, then calculates the ratio between them. This aldosterone-to-renin ratio helps distinguish whether high aldosterone is being driven by a problem in the adrenal glands themselves (primary) or by something upstream triggering excess renin production (secondary). For adults aged 18 to 99, the normal blood aldosterone range is roughly 3.1 to 35.4 nanograms per deciliter, according to Cleveland Clinic reference values, though results vary depending on the lab and the specific assay used.
For the initial screening blood draw, no special diet or posture preparation is required. Blood is simply drawn while you’re seated. If the screening ratio comes back elevated and confirmatory testing is needed, the process becomes more involved. One common confirmatory approach is oral salt loading, where you eat a high-sodium diet for three days before testing to see whether your body can appropriately suppress aldosterone production when it should. No single cutoff value is perfect for diagnosis, so clinicians interpret results in context alongside symptoms and sometimes imaging of the adrenal glands.
Medications That Block Aldosterone
For conditions involving excess aldosterone, doctors use a class of drugs called mineralocorticoid receptor antagonists, which block aldosterone from binding to its receptor. The two main options are spironolactone and eplerenone. Both compete with aldosterone at the same receptor site, preventing it from triggering sodium retention and potassium loss.
These medications are prescribed for a range of conditions beyond just primary hyperaldosteronism. They’re used to treat high blood pressure, reduce fluid buildup in liver disease and certain kidney conditions, and, increasingly, to protect the heart. In heart failure, adding one of these drugs to standard treatment has been shown to improve outcomes in patients with reduced heart pumping function. Current guidelines recommend them for patients with moderate to severe heart failure and for those who develop heart failure signs after a heart attack. Spironolactone tends to be the more commonly prescribed option, partly because it’s been available longer and costs less, though eplerenone causes fewer hormonal side effects like breast tenderness.
The most important thing to monitor while taking either drug is potassium levels. Since these medications block aldosterone’s potassium-flushing effect, potassium can build up in the blood, which is dangerous at high levels. Regular blood work is part of staying on these medications safely.