Aldosterone is a steroid hormone made in the outermost layer of the adrenal glands, called the zona glomerulosa. Its primary job is to help the kidneys maintain the right balance of sodium and potassium—two essential electrolytes—and, in doing so, regulate blood pressure and fluid volume. Aldosterone achieves this by acting on specific receptors in kidney cells, telling them to reabsorb sodium (and water with it) and to excrete potassium. This mechanism helps the body retain fluid during dehydration or blood loss, and helps prevent dangerous drops in blood pressure.
The release of aldosterone is tightly regulated by the renin-angiotensin system (RAS). This feedback loop begins when the kidneys sense low blood pressure or sodium levels, prompting them to release renin. Renin converts a protein called angiotensinogen into angiotensin I, which is then converted by angiotensin-converting enzyme (ACE) into angiotensin II. Angiotensin II, in turn, signals the adrenal glands to release aldosterone. High potassium levels and, to a lesser extent, the hormone ACTH (from the pituitary gland), can also stimulate aldosterone release.
Low aldosterone levels can occur in primary adrenal insufficiency (also known as Addison’s disease), where the adrenal glands are damaged and can’t produce enough hormones. This is often seen with autoimmune adrenalitis, and patients typically have low aldosterone and high renin, along with symptoms like low blood pressure, fatigue, salt craving, and high potassium (hyperkalemia). Early in this condition, aldosterone levels may drop before cortisol or ACTH levels become abnormal, making aldosterone a sensitive early marker.
In contrast, central adrenal insufficiency, caused by problems in the brain’s pituitary or hypothalamus (such as trauma or tumor), usually affects cortisol but not aldosterone. That’s because aldosterone is mainly regulated by the kidneys and angiotensin II, not ACTH. However, in very long-standing cases of central adrenal insufficiency, some decline in aldosterone function may still emerge.
Excess aldosterone, as seen in primary aldosteronism (Conn’s syndrome), leads to sodium retention, potassium loss, and high blood pressure. This condition used to be considered rare, but recent studies show it may be far more common than previously thought, especially among people with resistant or unexplained high blood pressure. The standard screening test involves measuring the aldosterone-to-renin ratio, which can uncover this hormonal imbalance even when routine blood pressure tests seem unremarkable.
Aldosterone also affects the heart and blood vessels. It can stiffen blood vessels by reducing nitric oxide (a molecule that helps them relax) and promote fibrosis (scarring) in the heart muscle. These effects make high aldosterone a risk factor for heart failure and stroke.