Hyperaldosteronism

With hyperaldosteronism, "hyper" means too much, and "aldosteronism" refers to the hormone aldosterone, which is made by the adrenal glands. So, hyperaldosteronism is a condition where the adrenal glands produce too much aldosterone.

Now, each of the two adrenal glands sits on top of a kidney and has two main parts.

The inner part, the medulla, produces the hormones epinephrine and norepinephrine.

On the flip side, the outer part, the cortex, has three layers. The innermost layer, the zona reticularis, produces androgens, such as dehydroepiandrosterone, which is a precursor of testosterone. The middle layer, the zona fasciculata, produces glucocorticoids, like cortisol. With glucocorticoids, “gluco-” refers to glucose, because they help increase blood glucose levels. The outermost layer, the zona glomerulosa, produces mineralocorticoids, such as aldosterone. With mineralocorticoids, “mineralo-” refers to minerals, because these hormones help regulate sodium and potassium levels. Now, the zona glomerulosa is controlled by the renin-angiotensin-aldosterone system.

When blood pressure or sodium levels drop, the juxtaglomerular cells in the kidneys release renin into the bloodstream. In the bloodstream, renin cleaves angiotensinogen into angiotensin I, which is later converted by angiotensin-converting enzyme or ACE, into angiotensin II.

Angiotensin II raises blood pressure through two mechanisms.

First, it triggers vasoconstriction of small arterioles, subsequently increasing peripheral vascular resistance. Second, angiotensin II stimulates the zona glomerulosa to release aldosterone.

Once in the bloodstream, aldosterone travels to the kidneys, more specifically, to the distal tubules and collecting ducts of the nephron.

Here, aldosterone squeezes into principal cells and stimulates mineralocorticoid receptors. When aldosterone activates mineralocorticoid receptors, the sodium-potassium pumps kick into high gear.
They begin to pump more sodium ions from the cell into the bloodstream.

This intracellular drop in sodium pulls more sodium from the tubule into the cell, following its concentration gradient. As sodium moves, water follows, so more water leaves the tubule and enters the blood vessels, eventually increasing blood volume and raising blood pressure.

At the same time, pumps pull potassium from the blood into the cells.

From here, potassium flows down its concentration gradient into the tubule to get excreted in the urine. That’s why another key trigger for the zona glomerulosa to release aldosterone is a high potassium level in the blood. Aldosterone helps the body remove extra potassium while holding on to sodium and water.

Now, based on the underlying pathology, hyperaldosteronism can be further subdivided into primary- and secondary types.

Primary hyperaldosteronism means that the adrenal glands are responsible for the excess production of aldosterone. The most common cause of primary hyperaldosteronism is bilateral idiopathic hyperaldosteronism. “Bilateral” means it affects both adrenal glands, and “idiopathic” means we’re not sure what’s causing it. But if we slice through the adrenal glands, we can recognize this condition by focal or widespread hyperplasia of cells that resemble those in the zona glomerulosa, which produce aldosterone.

Next, there are adrenocortical neoplasms.