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 glands1,2. 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.
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