Hyperaldosteronism: Causes, Dangers & Treatments

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  • 0:03 Raas and Aldosterone
  • 2:13 Causes and Effects
  • 6:04 Diagnosis and Treatment
  • 7:47 Lesson Summary
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Lesson Transcript
Instructor: Jennifer Szymanski

Jen has taught biology and related fields to students from Kindergarten to University. She has a Master's Degree in Physiology.

Aldosterone is one of many hormones necessary to help maintain water and sodium balance. In this lesson, we'll discuss hyperaldosteronism, the condition in which the body secretes too much of this important hormone.

RAAS and Aldosterone

'Salt' is often used as a synonym for 'flavor.' And indeed, the common sodium chloride that we shake, sometimes too liberally, onto our food makes the bland taste good. But sodium is also an essential nutrient, one that the body carefully regulates and keeps in balance with other electrolytes, especially potassium. In a condition called hyperaldosteronism (or sometimes just aldosteronism), the body makes too much of the steroid hormone aldosterone. As we'll see, aldosterone plays a major role in sodium, water, and potassium balance.

Let's start by reviewing just a little about this hormone and its pathway. Recall that aldosterone is part of a hormone system called the renin-angiotensin-aldosterone system, or RAAS. This system plays a large role in maintaining blood pressure. When the kidney senses low blood pressure, it secretes an enzyme called renin, which helps activate the hormone angiotensin. The final form of angiotensin stimulates the adrenal cortex, the outer layer of the adrenal gland, to release aldosterone.

Aldosterone is the steroid hormone that stimulates kidneys to absorb sodium ions. It also causes the kidneys to retain water (which happens by osmosis, since water follows high concentrations of solutes like sodium) and to excrete potassium and hydrogen ions. These actions raise blood pressure.

In addition to low blood pressure, aldosterone production is triggered by plasma acidosis (high concentration of hydrogen ions in the blood) and high potassium levels. When released, aldosterone binds to receptors in the nephron's distal tubule, turning on the sodium/potassium pumps there. Aldosterone isn't 'shut off' via a negative feedback loop. Instead, it stops being made when the body has absorbed enough sodium ions.

But what happens when the body makes too much aldosterone? And how does this condition happen in the first place?

Causes and Effects

Hyperaldosteronism (recall that 'hyper' means 'above') occurs any time the body makes too much aldosterone. It can be divided into two categories, primary and secondary.

Primary hyperaldosteronism results when something in the adrenal gland goes wrong. Sometimes called Conn's syndrome, primary hyperaldosteronism usually results from tumors of the adrenal gland called adenomas. Adrenal adenomas are benign - that is, they are non-cancerous - and form when adrenal epithelial cells don't stop dividing. These extra cells 'go rogue' and secrete aldosterone even when not stimulated by the RAAS.

Primary hyperaldosteronism can occur even when no adrenal tumor exists. This is termed idiopathic adrenal hyperplasia, which is a bit of a mouthful. It has a simple definition, though: an increased number of cells (there's 'hyper' again) in the adrenal gland for no determined reason.

These two classifications make up the majority of cases of primary hyperaldosteronism, with genetic conditions and cancerous adrenal tumors making up many of the rest of the cases.

Secondary hyperaldosteronism occurs when aldosterone secretion is cause by something other than the adrenal gland itself. Usually, this form of aldosteronism is associated with hypertension (high blood pressure) due to either some sort of kidney failure or tumors that secrete renin, kicking off the RAAS pathway. Liver cirrhosis, heart failure, and other conditions characterized by chronic low blood pressure (and therefore consistently trigger the RAAS) can also cause this type of aldosteronism.

Whatever the cause of hyperaldosteronism, the effects of the disease are similar. Let's go back to our picture of the nephron to see what happens when there's a lot of uncontrolled aldosterone floating around. The first thing that happens is that the RAAS is suppressed because sodium uptake is increased. Since the aldosterone acts on the distal tubule to increase sodium and water uptake into the blood and to force potassium and hydrogen excretion into the urine, there is a higher than normal blood sodium level called hypernatremia and a lower than normal blood potassium level called hypokalemia. (Notice how the letter 'K,' the chemical symbol for potassium, is right in that term, as well as the prefix 'hypo' - which means below or under, like a hypodermic needle goes below the skin.) Loss of hydrogen ions to the urine means the blood pH will also be basic, or alkaline.

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