The adrenal glands are small, cap-shaped organs situated atop the kidneys. Each gland is composed of an inner portion, the adrenal medulla, and an outer layer known as the adrenal cortex. The cortex is further subdivided into three distinct zones, each producing different types of steroid hormones. This article focuses on the outermost zone, the zona glomerulosa.
Anatomical Placement of the Glomerulosa
The zona glomerulosa is the most superficial layer of the adrenal cortex, lying directly beneath the connective tissue capsule. This layer constitutes approximately 15% of the total cortical volume. The cells are arranged in small, ovoid clusters or arches rather than in straight cords. This distinctive clustering pattern is the origin of the name glomerulosa, derived from the Latin word glomus meaning “ball.” Blood capillaries separate these cell clusters, facilitating the rapid release of synthesized hormones into the circulation.
The Principal Hormone Aldosterone
The primary steroid hormone produced by the zona glomerulosa is aldosterone, the main mineralocorticoid. Aldosterone is synthesized from cholesterol through a series of enzymatic conversions within the cells. The process begins with the transport of cholesterol into the mitochondria. The final step is catalyzed by the enzyme aldosterone synthase (CYP11B2). This enzyme is unique to the zona glomerulosa and enables the conversion of an intermediate steroid into the final product, aldosterone.
Managing Fluid and Electrolyte Balance
Aldosterone regulates fluid and electrolyte balance by targeting the cells of the kidney nephron. Its main site of action is the epithelial cells lining the distal convoluted tubules and the collecting ducts. Aldosterone binds to intracellular mineralocorticoid receptors, which act as transcription factors to influence gene expression. This action leads to the synthesis of new proteins that modulate the activity of ion transport systems.
The most notable effect is the promotion of sodium ion (\(\text{Na}^+\)) reabsorption back into the bloodstream. Aldosterone increases the activity of epithelial sodium channels (ENaCs) and sodium-potassium pumps (\(\text{Na}^+/\text{K}^+\)-ATPase) on the kidney cell membranes. This mechanism results in the retention of sodium and the accelerated excretion of potassium (\(\text{K}^+\)) and hydrogen ions (\(\text{H}^+\)).
Since water follows the osmotic gradient created by the reabsorbed sodium, this action leads to increased water retention and a rise in blood volume. The increase in blood volume contributes to an increase in blood pressure, making aldosterone a component in long-term blood pressure regulation. The excretion of hydrogen ions also contributes to the body’s acid-base balance.
Regulation by the Renin Angiotensin System
The secretion of aldosterone is primarily governed by the Renin-Angiotensin-Aldosterone System (RAAS). This cascade is initiated when the kidneys detect a drop in blood pressure or a decrease in sodium delivery. Specialized cells in the kidney release the enzyme renin into the bloodstream, which acts on angiotensinogen, converting it to angiotensin I.
Angiotensin I is converted to the active hormone angiotensin II (Ang II) by the Angiotensin-Converting Enzyme (ACE). Angiotensin II is the most potent and direct stimulus for the zona glomerulosa cells to synthesize and release aldosterone. It achieves this by binding to specific receptors, triggering a signaling cascade that increases the expression and activity of aldosterone synthase.
The zona glomerulosa is also responsive to the concentration of potassium in the blood plasma. Even a slight elevation in plasma potassium levels (hyperkalemia) directly stimulates the cells. The resulting influx of calcium ions activates the enzymes necessary for aldosterone synthesis and secretion. This direct potassium-sensing mechanism provides a swift negative feedback loop, ensuring potassium levels are lowered back into the normal range.