| Aldosterone is produced in the adrenal cortex and is the most potent mineralocorticoid in humans. Aldosterone secretion appears to be stimulated primarily through the renin-angiotensin system, in which decreased plasma sodium chloride concentrations lead to increased renin secretion and activation of angiotensin, with angiotensin II then stimulating aldosterone synthesis.
Aldosterone stimulates renal tubular sodium and chloride reabsorption, primarily at the level of the collecting ducts [1-4] and is important in the maintenance of blood pressure and blood volume. Aldosterone also enhances urinary potassium and hydrogen (acid) excretion.
Abnormally high plasma aldosterone levels are observed in primary hyperaldosteronism, in which renin levels are low, blood pressure is elevated and potassium levels are decreased [3,5]. Abnormally high aldosterone levels are also seen in secondary hyperaldosteronism as a result of elevated renin secretion [3,6]. Abnormally low aldosterone secretion occurs in a number of conditions including salt-wasting forms of congenital adrenal hyperplasia and renin deficiency [4,7,8].
References
1. Crabb J. Mol Cell Endocrinol 90:C11-C13, 1992.
2. Morris DJ. Endocrin Rev 2:234-247, 1981.
3. Kotchen TA & Guthrie GP Jr. Endocrin Rev 1:78-99, 1980.
4. Veldhuis JD & Melby JC. Endocrin Rev 2:495-517, 1981.
5. Bryer-Ash M, et al. Am J Dis Child 138:673-676, 1984.
6. Passwell J, et al. Acta Pdiatr Scand 73:127-130, 1984.
7. New MI & Levine LS: Congenital Adrenal Hyperplasia. (Monographs on Endocrinology, vol. 26) Springer-Verlag, Berlin, 1984.
8. Lee PDK, et al. J Clin Endocrinol Metab 62:225-229, 1986.
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