Aldosterone is a steroid hormone belonging to the mineralocorticoid class. It acts as a regulator of the body’s fluid and electrolyte balance, playing a foundational role in maintaining blood pressure and stable fluid volume. It achieves this by precisely controlling the concentration of sodium and potassium ions in the blood, ultimately conserving salt and water.
Where Aldosterone Originates and Acts
Aldosterone is synthesized and released by the adrenal glands, which are small organs located atop the kidneys. Specifically, it is produced in the outermost layer of the adrenal cortex, a region known as the zona glomerulosa. As a mineralocorticoid, its primary function is to influence mineral balance throughout the body.
The hormone acts on several epithelial tissues, but its most significant targets are the cells within the kidneys. Aldosterone primarily affects the principal cells located in the distal convoluted tubules and the cortical collecting ducts of the nephrons. It also exerts effects on the epithelial cells of the colon, salivary glands, and sweat glands, all aimed at conserving sodium.
The Intracellular Signaling Pathway
Aldosterone is a lipid-soluble steroid hormone, which allows it to pass directly across the lipid bilayer of the target cell membrane. Once inside the principal cell, it binds to a specific protein known as the intracellular mineralocorticoid receptor (MR). This binding event transforms the receptor into an activated hormone-receptor complex.
The activated complex then moves into the cell nucleus, where it functions as a transcription factor. It attaches to specific DNA sequences, initiating the transcription of target genes into messenger RNA (mRNA). This process, known as the genomic effect, leads to the translation of new proteins responsible for the hormone’s physiological effects.
The synthesized proteins include new ion channels and pumps inserted into the cell membranes. Aldosterone upregulates the production and activity of the Epithelial Sodium Channel (ENaC) on the apical membrane. It also increases the number and activity of the Na+/K+-ATPase pumps located on the basolateral membrane. This coordinated action enhances the cell’s capacity to transport sodium, making salt reabsorption the central event of the mechanism.
Systemic Effects on Fluid and Electrolyte Balance
The increased activity of ENaC channels and Na+/K+-ATPase pumps leads to three main physiological outcomes. First, it significantly increases the reabsorption of sodium ions from the tubular fluid back into the bloodstream. Sodium moves into the cell through ENaC and is then actively pumped out by the Na+/K+-ATPase, effectively conserving salt.
Second, the Na+/K+-ATPase pump draws potassium from the blood into the cell, which then diffuses into the tubular fluid for excretion. Aldosterone action thus causes a simultaneous increase in potassium excretion, regulating the body’s potassium concentration. This exchange of sodium conservation for potassium loss is a signature effect of the hormone.
The third effect is water retention, a passive consequence of sodium reabsorption. Water follows the conserved sodium ions out of the kidney tubules and back into the blood via osmosis, increasing extracellular fluid volume. This increase in fluid volume directly leads to higher blood volume, which raises systemic blood pressure.
How the Body Controls Aldosterone Release
The release of aldosterone is tightly regulated by a complex signaling cascade known as the Renin-Angiotensin-Aldosterone System (RAAS). This system is primarily activated when the body detects a drop in blood pressure or a decrease in sodium concentration. When blood flow to the kidneys is reduced, specialized cells release the enzyme renin into the bloodstream.
Renin acts on angiotensinogen, converting it to angiotensin I. This intermediate is then converted by Angiotensin-Converting Enzyme (ACE) into the potent hormone Angiotensin II. Angiotensin II is the primary hormonal signal that travels to the adrenal cortex to stimulate the release of aldosterone.
A second, non-RAAS factor influencing aldosterone secretion is the concentration of potassium in the blood. An elevation in blood potassium levels serves as a direct stimulus to the cells of the zona glomerulosa. This secondary mechanism ensures the hormone is released to regulate blood pressure and volume, and to promote the excretion of excess potassium.