ALDOSTERONE ELISA

BRAND:                 DEMEDITEC DIAGNOSTICS GMBH

PRODUCT CODE: DE4128

AVAILABILITY:     IN STOCK

DESCRIPTION

Rapid human ELISA kits for medical research and clinical use.

• Precoated ELISA plates and ready to use reagents

• Easy to use with fast, reliable and reproducible results

• CE certified for clinical diagnostic use

• Same day order processing and fast delivery

• UK based customer support

• ISO13485 certified manufacturer and distributor

ELISA specification

• 96 well ELISA microplate

• Incubation time: 1 h 20 min

• Range: 15 - 1000 pg/ml

• Sensitivity: 10 pg/ml

• Sample size: 50 µl

• Sample type: Serum, plasma, urine

• Substrate: TMB 450nm

Further information

Aldosterone produced in the adrenal cortex, is the most potent mineralocorticoid in humans. As with other steroid hormones, aldosterone is synthesized from cholesterol through a series of enzyme-mediated steps. Aldosterone and cortisol differ only in that a hydroxyl modification occurs at the 18, rather than 17, position on the steroid molecule.

The first and rate-limiting step in steroidogenesis, conversion of cholesterol to pregnenolone, is stimulated by adrenocorticotropic hormone (ACTH). However, ACTH has only a minimal effect on aldosterone production. Aldosterone secretion appears to be stimulated primarily through the renin-angiotensin system: decreased plasma volume and renal perfusion (or decreased plasma sodium chloride concentration) leads renin secretion and activation of angiotensin, with angiotensin II then stimulating aldosterone synthesis. Increased plasma potassium concentrations are also a strong independent stimulus for aldosterone production, although this effect is partially countered by potassium inhibition of renin release.

The major defined action of aldosterone is stimulation of renal tubular sodium and chloride reabsorption, primarily at the level of the collecting ducts. Other important renal actions include enhancement of urinary potassium and hydrogen (acid) excretion. Similar effects on transmembrane sodium and hydrogen transport have been observed in other tissues, including lymphocytes, brain and arterial smooth muscle. 

Plasma aldosterone levels normally vary with body position (upright>supine) and salt intake. Overall plasma aldosterone levels show a circadian rhythm which is similar but less marked than cortisol, with peak levels in the early morning. Age-related levels tend to decline from fetal through adult life. Aldosterone concentrations in urine and saliva have also been characterized.

Abnormally high plasma aldosertone concentrations can occur as either primary (e.g. in primary adenomas, glucocorticoid-responsive hypersaldosteroism, idiopathic) or secondary conditions. In primary hyperaldosteronism, renin levels are low, blood pressure is elevated and the potassium level is decreased. Secondary hyperaldosteronism occurs as a result of elevated renin secretion, and is observed in renovascular hypertension, renin-secreting tumors, intravascular volume depletion (dehydration), hypoadremia, and in Barther’s syndrome. High aldosterone and renin levels are also observed in pseudohypoaldosteronism, a condition caused by end-organ unresponsiveness to aldosterone leading to clinical features of aldosterone deficiencies.

Abnormally low aldosterone secretion occurs in a number of conditions including salt-wasting forms congenital adrenal hyperplasia, isolated 13-hydroxylase (carboxymethyl oxidase type  deficiency, renin deficiency (e.g. nephropathy), and type 4 renal tubular acidosis. Low aldosterone concentrations in the presence of clinical features of hyperaldosteronism can be observed in 11-hydroxylase (P450c11) deficiency, 11beta-hydroxysteroid dehydrogenase deficiency, and after ingestion of materials containing mineralocorticoid-like substances (e.g. licorice glycyntizic acid).