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Previous Volume 331:250-258 July 28, 1994 Number 4 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Patients with Addison's disease excrete excessive amounts of sodium in the urine but retain potassium, thus becoming hyponatremic and hyperkalemic. Early studies demonstrated that the problems could be ameliorated in humans and animals by administering extracts from adrenal glands^1,2. These extracts were presumed to contain hormones with sodium-retaining, or mineralocorticoid, properties. The existence of distinct mineralocorticoids was, however, not proved until a novel steroid with potent mineralocorticoid activity was isolated³. This hormone was named aldosterone to acknowledge its unique structural feature, an aldehyde group at C18.

This article reviews conditions of mineralocorticoid deficiency or excess, concentrating on primary . . . [Full Text of this Article]

Aldosterone Biosynthesis and Action

Regulation of Aldosterone Secretion

Metabolic Pathway of Aldosterone Biosynthesis

Action of Aldosterone

Mineralocorticoid Deficiency

Salt-Wasting Forms of Congenital Adrenal Hyperplasia

Aldosterone Synthase Deficiency

Other Inherited Disorders of Adrenal Function

Adrenal Insufficiency

Pseudohypoaldosteronism

Mineralocorticoid Excess

Primary Aldosteronism

Glucocorticoid-Suppressible Hyperaldosteronism

Hypersensitive Forms of Congenital Adrenal Hyperplasia

Apparent Mineralocorticoid Excess and Licorice Intoxication

Conclusions

Source Information

From the Divison of Pediatric Endocrinology, Cornell University Medical College, New York.

Address reprint requests to Dr. White at the Division of Pediatric Endocrinology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75235.

References

This article has been cited by other articles:

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