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The adrenal gland is responsible for producing two kinds of signaling molecules: steroid hormones, produced in the outer adrenal cortex, and catecholamines, generated in the adrenal medulla. Steroids can further be divided into mineralocorticoid (aldosterone), glucocorticoid (cortisol) and androgen (dehydroepiandrosterone [DHEA] and dehydroepiandrosterone-sulfate [DHEA-S]) classes. Each of these steroids is stereotypically produced by histologically differentiable cells in a particular layer of the adrenal cortex—the outermost zona glomerulosa produces aldosterone, the middle zona fasciculata produces cortisol, and the innermost zona reticularis produces DHEA and DHEA-S. Control of steroid hormone production and release, however, occurs outside of the adrenal gland; aldosterone is primarily controlled by the renin-angiotensin system and cortisol is regulated by adrenocorticotropic hormone (ACTH) from the pituitary gland, which itself is regulated by hypothalamic secretion of corticotropin-releasing hormone (CRH). Although DHEA-S is the most abundant androgen in serum, the control and function of DHEA and DHEA-S are less well understood.

Similar to the rest of the endocrine system, each of the steroid hormones produced by the adrenal gland can be pathologically elevated or pathologically absent. Specific to steroid producing tissues, two additional types of pathologies occur in the adrenal gland. The first is a defect in enzymatic activity leading to the absence of one steroid and to overproduction of a precursor steroid, with predictable off-target effects (e.g. congenital adrenal hyperplasia). The second defect is an alteration of timing of steroid production/release (e.g. premature adrenarche).


Hypothalamic CRH stimulates pituitary ACTH secretion. ACTH regulates adrenal glucocorticoid secretion and is secreted in a pulsatile fashion with amplitude that normally varies as a function of the time of day. This variation is the cause of the diurnal pattern of cortisol secretion. Cortisol secretion is highest early in the morning prior to waking, decreased in the afternoon to evening, and lowest at midnight, or 2 hours after sleep. Negative feedback on the synthesis and secretion of ACTH and CRH is provided by cortisol.1 In addition to this seemingly simple feedback loop, inflammation, via interleukin-6, stimulates ACTH production leading to cortisol secretion.


Mineralocorticoids maintain electrolyte equilibrium, stabilizing blood volume and blood pressure. They control sodium reabsorption in exchange for potassium in the distal tubule of the kidney. Glucocorticoids are “stress hormones,” and thus they have metabolic activities increasing glucose availability in seemingly counterintuitive ways. They have catabolic effects—increasing protein degradation in muscle, skin, and peripheral adipose tissue, and anabolic effects—enhancing the ability for gluconeogenesis at the liver and increasing central fat storage. In addition, glucocorticoids are permissive for the vasoconstrictive actions of catecholamines.1 Synthetic analogues of glucocorticoids demonstrate variable anti-inflammatory/gluconeogenic activity, and have variable salt-retaining properties. Androgens promote the growth of pubic and axillary hair.


Aldosterone production and secretion is regulated by renin, and to a lesser degree, serum potassium levels.2 Renin ...

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