Notes
Aldosterone Physiology
Sections
Key points
Aldosterone is the primary mineralocorticoid and is secreted from the zona glomerulosa.
For more on the biosynthesis of aldosterone, click here: adrenal cortex hormones
Aldosterone maintains body fluid and electrolyte homeostasis.
Its secretion is regulated primarily by angiotensin II, serum potassium levels, and ACTH.
We can distinguish between two forms of hyperaldosteronism, depending on the cause:
- In primary hyperaldosteronism, excessive secretion from the adrenal gland is autonomous; for example, an aldosterone-secreting tumor.
- In secondary hyperaldosteronism, excessive aldosterone secretion is the result of excessive renin secretion.
Hyperaldosteronism is an important cause of secondary hypertension – thus, detection and treatment are key to minimizing cardiovascular damage.
Treatment can be surgical or medical.
Physiology
In a healthy individual, aldosterone maintains normal blood volume and electrolyte balance.
Key anatomical structures in the renin-angiotensin II- aldosterone feedback loop:
- The kidney, which senses changes in blood pressure.
- Nephron with the glomerulus and the presence of the juxtaglomerular cells near the afferent arteriole (click here for glomerular details).
- Liver and indicate that it produces angiotensinogen.
- Lungs; their vascular endothelium is an important site for production of angiotensin converting enzyme (ACE).
- Adrenal gland and show that it produces aldosterone.
- Low blood volume produces reduced renal perfusion pressure.
In response, the juxtaglomerular cells release renin, which is the enzyme that converts angiotensinogen to angiotensin I. - ACE then converts angiotensin I to angiotensin II, which triggers release of aldosterone from the adrenal gland.
- Aldosterone increases the insertion of ENaCs (epithelial sodium channels) in the distal nephron.
- As a result, sodium and water retention increases.
- In turn, sodium reabsorption produces a negative electrochemical gradient that allows for potassium and, ultimately, hydrogen ion loss (for a review of reabsorption and secretion in the nephron, see the links in our notes).
- Because sodium and water are retained, blood volume increases.
In a healthy person, the return to normotension will "turn off" juxtaglomerular renin release.
Some additional stimuli and inhibitors for aldosterone secretion:
- Hyperkalemia, ACTH, and catecholamine-stimulated release of renin trigger aldosterone release.
- Hypokalemia, atrial natriuretic peptide (ANP), dopamine, and heparin inhibit aldosterone release.
Hyperaldosteronism - Excessive aldosterone secretion.
References
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