Aldosterone: role in controlling renal excretion

2021-05-06 09:39 AM

In the complete absence of aldosterone, volume depletion can be severe unless the person is allowed to eat a lot of salt and drink plenty of fluids to balance the increased salt and water in the urine.

Aldosterone increases sodium reabsorption, especially in the tubules of the renal cortex. An increase in sodium reabsorption is also associated with increased water reabsorption and potassium excretion. Therefore, the real effect of aldosterone is to cause the kidneys to retain sodium and water, but also increase urinary excretion of potassium.

The function of aldosterone in regulating sodium balance is closely related to the function described for Angiotensin II. That is, with a decrease in sodium intake, Angiotensin II levels increase, stimulating aldosterone secretion, thereby contributing to a decrease in urinary sodium excretion and, therefore, maintaining sodium balance. In contrast, with high sodium content, inhibition of aldosterone formation reduces tubular reabsorption, allowing the kidneys to excrete larger amounts of sodium. Therefore, changes in aldosterone formation also aid in the mechanism of pressure sodium diuresis in maintaining sodium balance during salt intake alterations.

During chronic Aldosterone secretion, the Kidneys "Escape" from Sodium Retention as Arterial Pressure Increases. Although aldosterone has a strong effect on sodium reabsorption when too much aldosterone is infused or too much aldosterone is formed, as occurs in patients with tumours of the adrenal gland (Conn syndrome), the reabsorption increases. Sodium and decreased renal sodium excretion are only transient.

After 1 to 3 days of sodium and water retention, the extracellular fluid volume increases by about 10 to 15 percent and at the same time, there is an increase in arterial blood pressure.

When the arterial pressure is increased enough, the kidneys "escape" from sodium retention and water retention, and then excrete as much sodium as the daily intake, despite the constant presence of high aldosterone. The main reason is due to diuretic and sodium diuresis that occurs when arterial pressure is increased.

In patients with impaired adrenal insufficiency that does not secrete enough aldosterone (Addison's disease), there is increased excretion of sodium and water, decreased extracellular fluid volume, and a tendency to low blood pressure.

In the complete absence of aldosterone, volume depletion can be severe unless the person is allowed to eat a lot of salt and drink plenty of fluids to balance the increased salt and water in the urine.



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