QS Study

Aldosterone is produced in the cortex of the adrenal glands, which are located above the kidneys. It is essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon. It affects the body’s ability to regulate blood pressure. It balances the levels of sodium and potassium in your body. It plays an essential role in salt–water balance by acting on epithelial mineralocorticoid receptors (MR).

Aldosterone escape

Prolonged mineral corticoid excess leads to K+ depletion due to prolonged K+ diuresis. H+ is also retained initially. But Na+ is retained initially, but the plasma Na+ is elevated only slightly because water is retained with the osmotically active Na+. This phenomenon is considered to be an important homeostatic mechanism and thought to be dependent on nitric oxide.

Consequently, ECF volume is expanded and the BP rises. When the ECF expansion passes a certain point. Na+ excretion is usually increased in spite of continued action of mineral corticoids on the renal tubules.

This phenomenon is called “Aldosterone escape’ or ‘Escape phenomenon’. It is in the treatment of heart failure with angiotensin-converting enzyme inhibitors.

Fig: Mechanisms of aldosterone escape during AT1-receptor blockade or ACE-inhibition

Aldosterone escape is a phenomenon which occurs in primary hyperaldosteronism. It refers to the escape from the salt and water retaining effects of aldosterone.

It does not work in the aldosterone excess of edematous conditions like congestive heart failure and cirrhosis liver, perhaps due to the renal hypoperfusion, which is not a feature of major aldosteronism.