Mineralocorticoid

Mineralocorticoids are a group of hormones produced in the adrenal cortex, with aldosterone being the principal mineralocorticoid. This group is primarily associated with the water and electrolyte balance. This is accomplished through the effect on ion transport in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by plasma volume, serum potassium, and angiotensin II.

The reabsorption of sodium in the kidneys controls blood volume. If there is a decrease in blood flow or blood volume in the kidney, the kidney releases renin, which in turn acts on the hormone angiotensin, to increase aldosterone level.

The major physiologic regulator of aldosterone levels is the renin-angiotensin system. Renin, synthesized in the kidney, converts angiotensinogen to angiotensin I (AT I). The AT I peptide is subsequently converted to the active peptide angiotensin II (AT II) and its bioactive degradation products AT III and AT IV, by the action of angiotensin-converting enzymes (ACE). AT II (and probably AT III and AT IV) stimulates aldosterone biosynthesis through interaction with G-protein coupled receptors in the zona glomerulosa. This process is regulated by a variety of factors including plasma potassium level, intracellular calcium, and release of nitric oxide (NO) and atrial natriuretic peptide. AT II also increases peripheral arterial resistance, which results in increased blood pressure. Changes in blood pressure then feed back on the secretion of renin, a process regulated by the interaction of kidney baroreceptors, renal nerves, NO synthesis, and the balance of calcium, potassium, and sodium in the serum.

Sodium and potassium levels are another modulator of mineralocorticoid synthesis. Increased serum potassium directly impacts the adrenal gland, upregulating early steps in adrenal steroid biosynthesis and resulting in increased aldosterone secretion. Low serum sodium can also increase aldosterone secretion, but this mechanism does not appear to be a major regulator of mineralocorticoid secretion, because serum sodium concentration changes little with changes in total blood volume.