[6] It plays a central role in the homeostatic regulation of blood pressure, plasma sodium (Na+), and potassium (K+) levels.

It does so primarily by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron.

Another example is spironolactone, a potassium-sparing diuretic of the steroidal spirolactone group, which interferes with the aldosterone receptor (among others) leading to lower blood pressure by the mechanism described above.

Aldosterone tends to promote Na+ and water retention, and lower plasma K+ concentration by the following mechanisms: Aldosterone is responsible for the reabsorption of about 2% of filtered sodium in the kidneys, which is nearly equal to the entire sodium content in human blood under normal glomerular filtration rates.

This enzyme co-localizes with intracellular adrenal steroid receptors and converts cortisol into cortisone, a relatively inactive metabolite with little affinity for the MR. Liquorice, which contains glycyrrhetinic acid, can inhibit 11β-HSD and lead to a mineralocorticoid excess syndrome.

[23] A small portion of the regulation resulting from angiotensin II must take place indirectly from decreased blood flow through the liver due to constriction of capillaries.

Although sustained production of aldosterone requires persistent calcium entry through low-voltage-activated Ca2+ channels, isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca2+ channels entry.

[25] However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of zona glomerulosa cells provides a platform for the production of a recurrent Ca2+ channels signal that can be controlled by angiotensin II and extracellular potassium, the 2 major regulators of aldosterone production.

[26] The amount of plasma renin secreted is an indirect function of the serum potassium[27][28] as probably determined by sensors in the carotid artery.

[31] Aldosterone is increased by blood loss,[32] pregnancy,[33] and possibly by further circumstances such as physical exertion, endotoxin shock, and burns.

[34][35] The aldosterone production is also affected to one extent or another by nervous control, which integrates the inverse of carotid artery pressure,[29] pain, posture,[33] and probably emotion (anxiety, fear, and hostility)[36] (including surgical stress).

[38] Thus, there is an advantage to an animal's anticipating a future need from interaction with a predator, since too high a serum content of potassium has very adverse effects on nervous transmission.

[40] Aldosterone levels vary as an inverse function of sodium intake as sensed via osmotic pressure.

The most common cause of this condition (and related symptoms) is Addison's disease; it is typically treated by fludrocortisone, which has a much longer persistence (1 day) in the bloodstream.