Gold serum separator (SST) tube
Spin and separate
Refrigerated (preferred) - 14 days
Ambient - 3 days
Frozen - 14 days
Freeze/thaw cycles - stable x 3
Liquid chromatography/tandem mass spectrometry (LC/MS-MS)
0 - 2 years: See report
2 - 9 years: 5.0−80.0 ng/dL
10 - 14 years: 4.0−48.0 ng/dL
>14 years: 0.0−30.0 ng/dL
The renin-angiotensin system and potassium ion are the major regulators of aldosterone secretion, whereas ACTH and other POMC peptides, sodium ion, vasopressin, dopamine, ANP, α-adrenergic agents, serotonin, and somatostatin are minor modulators. Renin cleaves angiotensinogen, which is synthesized by the liver; to produce angiotensin I. Angiotensin I is, in turn, rapidly cleaved by angiotensin-converting enzyme (ACE) in the lung and other tissues to form angiotensin II. Angiotensin II stimulates aldosterone secretion and vasoconstriction. Factors that decrease renal blood flow, such as hemorrhage, dehydration, salt restriction, upright posture, and renal artery narrowing, increase renin levels which, in turn, raise aldosterone levels. In contrast, factors that increase blood pressure, such as high salt intake, peripheral vasoconstrictors and supine posture, decrease renin and aldosterone levels. Aldosterone promotes active sodium transport and excretion of potassium.
Hypokalemia increases and hyperkalemia decreases renin release. Potassium also directly increases aldosterone secretion by the adrenal cortex and aldosterone then lowers serum potassium by stimulating its excretion by the kidney. High dietary potassium intake increases plasma aldosterone and enhances the aldosterone response to a subsequent potassium or angiotensin II infusion.
Primary hyperaldosteronism, also referred to as Conn syndrome, is caused by the overproduction of aldosterone by one or both of the adrenal glands. Historically, primary aldosteronism was considered to be an uncommon cause of hypertension. However, recent studies indicate that 10% to 15% of cases are associated with primary hyperaldosteronism. Secondary hyperaldosteronism is relatively common and can occur as the result of any condition that decreases blood flow to the kidneys (ie, renal artery stenosis), decreases blood pressure, or lowers plasma sodium levels. Secondary hyperaldosteronism may also be seen with cirrhosis, congestive heart failure, and toxemia of pregnancy.
Hyperaldosteronism increases reabsorption of sodium and loss of potassium by the kidneys, resulting in an electrolyte imbalance. The condition can be asymptomatic, although muscle weakness can occur if potassium levels are very low. A number of studies have suggested that high-normal aldosterone levels predict development of high blood pressure in normotensive subjects6 and that increased aldosterone action contributes to hypertension, cardiovascular fibrosis, and cardiac hypertrophy.