Aldosterone action on the distal nephron
Aldosterone is a steroid hormone that makes the late nephron (the later part of the kidney's filtering tube) keep sodium and lose potassium, so water follows.
Remember
Aldosterone makes the later parts of the nephron keep sodium and lose potassium, and water follows the sodium, so blood volume and blood pressure rise.
Aldosterone is the main mineralocorticoid, a steroid hormone made in the outermost layer of the adrenal cortex (the outer part of the adrenal gland) that controls salt balance. In the kidney it controls how much sodium is reabsorbed and how much potassium is lost.
It acts on the principal cells (the main salt-handling cells) of the distal convoluted tubule and collecting duct, the last stretches of the nephron. Because it is a steroid, it enters the cell and binds the mineralocorticoid receptor (a receptor inside the cell that carries the hormone to the nucleus). The cell then makes more sodium channels and more sodium-potassium ATPase pumps (pumps in the cell membrane that swap sodium out for potassium).
Sodium moves from the urine into the cell and on into the blood, and potassium is lost into the urine in exchange. Water follows the sodium by osmosis, so blood volume expands and blood pressure rises. Aldosterone does not control the water channels itself: antidiuretic hormone (also called vasopressin) does that, in a separate pathway that responds to how concentrated the blood is.
Aldosterone release is mainly driven by the renin-angiotensin-aldosterone system (RAAS), the kidney's response to a fall in blood volume or pressure.
In primary hyperaldosteronism (too much aldosterone from a defect in the adrenal cortex), blood pressure is high, and the potassium loss can cause hypokalaemia (a low blood potassium). Renin, the enzyme the kidney releases when blood volume or pressure is low, is low in this condition, because the rise in volume and pressure switches off renin release. In secondary hyperaldosteronism, the excess aldosterone is due to overactivity of the RAAS, so renin is high.
Key facts
- Site
- principal cells of the distal convoluted tubule and collecting duct.
- Ions
- sodium is reabsorbed and potassium is lost into the urine in exchange.
- Water
- it follows the sodium by osmosis (water moving towards the saltier fluid), so blood volume and blood pressure rise.
- Excess aldosterone
- high blood pressure, and the potassium loss can cause hypokalaemia (a low blood potassium).
- Renin
- low in primary hyperaldosteronism and high in secondary hyperaldosteronism.
- Treatment of hyperaldosteronism
- it depends on the cause; surgery can be used for an aldosterone-secreting adrenal tumour, or spironolactone (a mineralocorticoid receptor antagonist) can be used for other causes.
Exam traps
- Aldosterone does increase sodium reabsorption and potassium excretion, but it does so in the distal convoluted tubule and collecting duct, not in the proximal tubule (the first part of the nephron), so the right ions in the wrong site still make a wrong statement.
- Water channels in the collecting duct are regulated by antidiuretic hormone, not by aldosterone, which increases water reabsorption only indirectly, because water follows the sodium it retains.
- Aldosterone does not make the kidney keep both sodium and potassium. It increases potassium excretion, which is why an excess can cause hypokalaemia (a low blood potassium).
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