Aldosterone is a steroid hormone (mineralocorticoid family) produced by the outer-section (zona glomerulosa) of the adrenal cortex in the adrenal gland to regulate sodium and potassium balance in the blood. It is synthesized from cholesterol by aldosterone synthase, which is absent in other sections of the adrenal gland.

It is the sole endogenous member of the class of mineralocorticoids in human. It functions in two main locations of the kidney:

At distal tubule:     Acting on mineralocorticoid receptors (MR) on principal cells in the distal tubule of the kidney nephron, it increases the permeability of their apical (luminal) membrane to potassium and sodium and activates their basolateral Na+/K+ pumps, stimulating ATP hydrolysis, reabsorbing sodium (Na+) ions and water into the blood, and excreting potassium (K+) ions into the urine.  

At collecting duct: Aldosterone also stimulates H+ secretion by α-intercalated cells in the collecting duct, regulating plasma bicarbonate (HCO3-) levels and its acid/base balance.

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 GFR (glomerular filtration rate).  

Aldosterone synthesis is stimulated by several factors:
? by increased plasma angiotensin II, ACTH, or potassium levels, which are present in proportion to plasma sodium deficiencies
? by plasma acidosis
? by the stretch receptors located in the atria of the heart. If decreased blood pressure is detected, the adrenal gland is stimulated by these stretch receptors to release aldesterone, which increases sodium reabsorption from the urine, sweat and the gut. This causes increased osmolarity in the extracellular fluid which will eventually return blood pressure toward normal.  

Plasma aldosterone levels show a circadian rhythm, which is similar to but less marked than cortisol, with peak levels in the early morning; about 75% of the daily production is secreted between 04:00 am and 10:00 am each day. Age-related levels tend to decline from fetal through adult life.

Abnormal high plasma aldosterone concentrations can occur in adenomas, glucocorticoid-responsive hyperaldosteronism, idiopathic. Abnormal low aldosterone secretion occurs in a number of conditions including salt-wasting forms of congenital adrenal hyperplasia, nephropathy, and renal tubular acidosis.

May be diagnosed by:

• Determination of specific antibodies based on the ELISA technique
• Determination of specific antibodies based on the RIA-technique

Aldosterone ELISA:

The Aldosterone ELISA is intended for competitive immunoenzymatic colorimetric method for quantitative determination of Aldosterone in human serum or plasma.

Principle of the Assay:

Microtiter strip wells are precoated with anti-Aldosterone antibodies (solid-phase). Aldosterone in the sample competes with biotinylated Aldosterone-Streptavidin-HRP conjugate for antibody binding. After incubation a bound/free separation is performed by solid-phase washing. The formed immune complex is visualized by adding Tetramethylbenzidine (TMB) substrate which gives a blue reaction product. The intensity of this product is inversely proportional to the amount of Aldosterone in the sample. Sulphuric acid is added to stop the reaction. This produces a yellow endpoint colour. Absorption at 450 nm is read using an ELISA microwell plate reader.

Specific performance characteristics: 

Correlation with RIA performed on 92 samples is r = 0.88

Order information: