Aldosterone is a hormone that controls how much sodium and water your body holds onto, which directly regulates your blood pressure and potassium levels. It’s produced in a specific outer layer of your adrenal glands (small organs sitting on top of each kidney) and acts primarily on your kidneys, telling them to reabsorb sodium back into the bloodstream instead of letting it leave in urine. That retained sodium pulls water with it, increasing blood volume and raising blood pressure.
Where Aldosterone Is Made
Your adrenal glands have three distinct layers, each producing different hormones. Aldosterone comes from the outermost layer, called the zona glomerulosa, where cells are arranged in small clusters just beneath the gland’s outer capsule. These cells contain a specialized enzyme called aldosterone synthase that converts precursor molecules into aldosterone. No other cells in the body produce this enzyme in meaningful amounts, which is why aldosterone production is so tightly localized.
What Triggers Its Release
Two main signals tell your adrenal glands to ramp up aldosterone production, and they work independently of each other.
The first is a cascade called the renin-angiotensin-aldosterone system. When your blood pressure drops or blood flow to the kidneys decreases, specialized kidney cells release an enzyme called renin. Renin sets off a chain reaction that ultimately produces a molecule called angiotensin II, which travels to the adrenal glands and stimulates aldosterone release. This is the body’s primary mechanism for recovering from low blood pressure, dehydration, or blood loss.
The second trigger is potassium. When potassium levels in the blood rise even slightly, the zona glomerulosa cells respond directly by ramping up aldosterone production. This happens through calcium channels on the cell surface that open in response to higher potassium concentrations. In lab studies, aldosterone secretion increases roughly 4-fold as potassium rises from low to moderately high levels. This pathway operates completely independently of renin, giving the body a second, parallel way to fine-tune aldosterone output.
Aldosterone also follows a daily rhythm. Levels peak at the end of the biological night and into early morning, then decline through the afternoon and evening. This rhythm persists even when people are kept awake continuously, meaning it’s driven by the body’s internal clock rather than by sleep itself.
How It Works Inside Cells
Once aldosterone enters the bloodstream, it reaches its target cells, primarily in the kidneys. But unlike hormones that attach to receptors on the outside of a cell, aldosterone is small and fat-soluble enough to pass directly through cell membranes. Inside the cell, it binds to a protein called the mineralocorticoid receptor.
This binding changes the receptor’s shape, causing it to fold into a compact configuration that exposes a surface groove. That groove attracts helper proteins called coactivators, which latch on and prepare the receptor complex to enter the cell’s nucleus. Once inside the nucleus, the activated receptor attaches to specific stretches of DNA and switches on particular genes. Those genes encode the proteins that actually carry out aldosterone’s effects: ion channels and pumps that move sodium, potassium, and water across kidney cells.
One important detail: cortisol, the body’s main stress hormone, can also bind to this same receptor. But the binding triggers only a very weak activation compared to aldosterone. Kidney cells contain a protective enzyme that breaks down cortisol before it can occupy the mineralocorticoid receptor, ensuring aldosterone’s signal comes through clearly despite cortisol circulating at much higher concentrations.
What It Does in the Kidneys
Aldosterone’s most important job happens in a section of the kidney tubule called the distal nephron, the final stretch of the tiny tubes that filter and refine urine. Here, aldosterone controls three key proteins that work together like a coordinated system.
The first is the epithelial sodium channel, or ENaC, which sits on the inner surface of kidney cells facing the urine. Aldosterone increases the number of these channels present in the cell membrane. More channels mean more sodium gets pulled out of the urine and back into the cell. The rate of sodium reabsorption in this part of the kidney correlates directly with aldosterone levels in the blood and inversely with how much sodium you’re eating.
The second is a pump on the opposite side of the same cells, facing the bloodstream. This sodium-potassium pump pushes sodium out of the cell and into the blood while pulling potassium in the other direction. Aldosterone increases its activity, creating a continuous conveyor belt: sodium enters the cell from the urine side through ENaC, then gets pushed into the blood by the pump.
The third is a potassium channel called ROMK, also facing the urine side. As the sodium-potassium pump loads cells with potassium, ROMK channels allow that potassium to flow out into the urine. Aldosterone increases the number of ROMK channels at the cell surface, which is why aldosterone ultimately causes potassium loss in urine. This is the mechanism behind aldosterone’s role as a potassium regulator: it trades sodium retention for potassium excretion.
There’s also a sodium-chloride cotransporter earlier in the distal tubule that aldosterone activates, adding another route for sodium reclamation. Together, these proteins give aldosterone control over a significant fraction of the sodium and potassium that passes through your kidneys each day.
The Effect on Blood Pressure
Sodium reabsorption doesn’t just change the composition of your urine. When sodium moves back into the bloodstream, water follows it by osmosis. This increases your total blood volume, which in turn raises blood pressure. In a healthy person, this is a precisely calibrated feedback loop: low blood pressure triggers renin, renin leads to aldosterone, aldosterone retains sodium and water, blood pressure rises, and the signal to produce renin shuts off.
The system becomes damaging when aldosterone stays elevated despite normal or high sodium levels. Researchers have noted that aldosterone levels “inappropriate for sodium status” cause cardiovascular harm, while much higher aldosterone levels during genuine sodium deficiency are perfectly safe and protective. The difference is context. When aldosterone is doing its job in response to real sodium depletion, it’s homeostatic. When it’s elevated for the wrong reasons, the excess sodium and water retention drives sustained high blood pressure and damages blood vessels.
When the System Goes Wrong
The most common disorder of aldosterone overproduction is called primary aldosteronism. In this condition, one or both adrenal glands produce too much aldosterone regardless of whether the body needs it. Because the overproduction doesn’t come from the renin pathway, renin levels are characteristically low while aldosterone runs high.
Screening involves measuring the ratio of aldosterone to renin in the blood. A ratio above 20 (using standard units) combined with suppressed renin and an aldosterone level at or above 10 ng/dL suggests the diagnosis. For reference, normal aldosterone in adults ranges from about 3 to 35 ng/dL depending on sodium intake, body position, and time of day.
The hallmark symptoms reflect exactly what you’d predict from aldosterone’s mechanism: high blood pressure that’s often resistant to standard medications, and low potassium levels that can cause muscle weakness, cramping, or fatigue. Some people have no obvious symptoms beyond stubborn hypertension, which is why screening is recommended in people whose blood pressure doesn’t respond well to treatment.
On the opposite end, too little aldosterone (as occurs in Addison’s disease or adrenal insufficiency) leads to the reverse problem: the kidneys can’t hold onto enough sodium, blood pressure drops, and potassium climbs to potentially dangerous levels. This makes aldosterone one of the few hormones where both excess and deficiency produce clearly recognizable, opposite clinical pictures, all traceable to the same sodium-potassium exchange mechanism in the kidney.