Aldosterone is a steroid hormone, classified as a mineralocorticoid, produced by the outer layer of the adrenal glands, which sit atop the kidneys. Its primary responsibility is managing the body’s internal environment by regulating the concentration of mineral electrolytes, particularly sodium and potassium, within the bloodstream. By maintaining this precise balance, aldosterone exerts a profound influence on fluid volume and blood pressure throughout the circulatory system.
Primary Function in Fluid and Electrolyte Balance
Aldosterone primarily acts within the kidneys, targeting the principal cells of the late distal tubules and collecting ducts. The hormone signals these cells to increase the active reabsorption of sodium ions (\(\text{Na}^+\)) from the filtered fluid back into the bloodstream. This mechanism effectively conserves the body’s sodium supply, earning aldosterone the designation of a salt-retaining hormone.
Because water passively follows sodium, the increased sodium reabsorption directly leads to greater water retention by the body. This retention of salt and water increases the overall volume of fluid circulating in the blood vessels, which serves to support or raise blood pressure. Simultaneously with sodium uptake, aldosterone promotes the secretion of potassium ions (\(\text{K}^+\)) and hydrogen ions (\(\text{H}^+\)) into the tubular fluid destined to become urine.
This exchange conserves sodium at the expense of potassium and hydrogen excretion. The movement of potassium out of the body prevents dangerously high potassium levels in the blood. Furthermore, the excretion of hydrogen ions contributes to the regulation of the body’s acid-base balance, helping to keep blood pH within a healthy range.
How the Body Regulates Aldosterone Production
The body’s control over aldosterone release centers around the complex signaling pathway called the Renin-Angiotensin-Aldosterone System (RAAS). This system is primarily activated when the body senses a drop in blood pressure or a reduction in the blood’s sodium concentration. In response to these changes, specialized cells in the kidneys release the enzyme renin into the circulation.
Renin acts on a protein produced by the liver, converting it into angiotensin I. As angiotensin I passes through the lungs and kidneys, Angiotensin-Converting Enzyme (ACE) transforms it into Angiotensin II. Angiotensin II is the main signal that travels to the adrenal glands, stimulating the outer layer to synthesize and release aldosterone.
High levels of potassium in the blood also serve as a direct stimulus for the adrenal glands to secrete aldosterone, independent of the RAAS. This mechanism acts as a rapid feedback loop to ensure that excess potassium is quickly removed from the circulation. The system works to adjust fluid and electrolyte levels, ensuring that blood volume and pressure remain stable.
Health Consequences of Abnormal Aldosterone Levels
Dysregulation of aldosterone production leads to two primary states: hyperaldosteronism (excessive hormone levels) and hypoaldosteronism (insufficient levels). Hyperaldosteronism, often called Conn’s Syndrome when caused by an adrenal gland issue, results in the continuous over-retention of sodium and water. This chronic fluid overload is a major cause of high blood pressure (hypertension) that is often resistant to conventional drug treatments.
The excessive aldosterone also drives the excretion of potassium, leading to hypokalemia, or low potassium levels in the blood. Symptoms associated with hypokalemia include:
- Generalized muscle weakness.
- Fatigue.
- Numbness.
- Irregular heart rhythm.
Long-term, uncontrolled hyperaldosteronism significantly increases the risk for cardiovascular events, including stroke, heart failure, and kidney damage.
Conversely, hypoaldosteronism involves a deficit of the hormone, preventing the kidneys from effectively conserving sodium and water. This inability to retain fluid results in a reduction of circulating blood volume, which often manifests as low blood pressure (hypotension). The lack of aldosterone also impairs the kidney’s ability to excrete potassium and hydrogen ions.
This deficit causes hyperkalemia (high potassium levels), which affects heart function, and may also lead to low sodium levels (hyponatremia). Causes of hypoaldosteronism include primary adrenal insufficiency, such as Addison’s disease, or specific enzyme deficiencies that impede hormone synthesis. Symptoms often include low blood pressure, persistent fatigue, and salt cravings.
Medical Management of Aldosterone Disorders
Treatment for hyperaldosteronism depends on its underlying cause, focusing on counteracting the hormone’s effects or removing the source of its overproduction. When the condition is caused by a non-cancerous tumor on one adrenal gland, surgical removal (adrenalectomy) is often the curative option. For cases where both adrenal glands are overactive or when surgery is not feasible, medication is used to block the hormone’s action.
Doctors commonly prescribe Mineralocorticoid Receptor Antagonists (MRAs), such as spironolactone or eplerenone, which prevent aldosterone from binding to its receptor sites in the kidney. This blockade reverses the electrolyte imbalance, helping to lower blood pressure and restore potassium levels to normal. Eplerenone is sometimes preferred as it has a lower risk of causing certain side effects compared to spironolactone.
For patients with hypoaldosteronism, the primary therapeutic strategy involves hormone replacement to restore mineralocorticoid activity. The synthetic steroid fludrocortisone is the standard medication used to mimic the actions of natural aldosterone. This treatment helps the kidneys retain sodium and water, supporting blood volume and blood pressure while also facilitating potassium excretion. Patients on fludrocortisone may also be advised to increase their dietary salt intake.