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Overview of Adrenal Function

By Ashley B. Grossman, MD, FRCP, FMedSci

The adrenal glands, located on the cephalad portion of each kidney, consist of a cortex and medulla, each with separate endocrine functions.


The adrenal cortex produces glucocorticoids (primarily cortisol), mineralocorticoids (primarily aldosterone), and androgens (primarily dehydroepiandrosterone and androstenedione). The physiology of the hypothalamic-pituitary-adrenocortical system is further discussed in Overview of the Endocrine System.

Glucocorticoids promote and inhibit gene transcription in many cells and organ systems. Prominent effects include anti-inflammatory actions and increased hepatic gluconeogenesis.

Mineralocorticoids regulate electrolyte transport across epithelial surfaces, particularly renal conservation of Na in exchange for K.

Adrenal androgens’ chief physiologic activity occurs after conversion to testosterone and dihydrotestosterone.


The adrenal medulla is composed of chromaffin cells, which synthesize and secrete catecholamines (mainly epinephrine and lesser amounts of norepinephrine ). Chromaffin cells also produce bioactive amines and peptides (eg, histamine, serotonin, chromogranins, neuropeptide hormones). Epinephrine and norepinephrine , the major effector amines of the sympathetic nervous system, are responsible for the “flight or fight” response (ie, chronotropic and inotropic effects on the heart; bronchodilation; peripheral and splanchnic vasoconstriction with skeletal muscular vasodilation; metabolic effects including glycogenolysis, lipolysis, and renin release).

Clinical syndromes

Most deficiency syndromes affect output of all adrenocortical hormones. Hypofunction may be primary (malfunction of the adrenal gland itself, as in Addison disease—see page Addison Disease) or secondary (due to lack of adrenal stimulation by the pituitary or hypothalamus, although some experts refer to hypothalamic malfunction as tertiary).

Hyperfunction causes distinct clinical syndromes. Hypersecretion of androgens results in adrenal virilism (see page Adrenal Virilism); of glucocorticoids, Cushing syndrome (see page Cushing Syndrome); and of aldosterone, hyperaldosteronism (aldosteronism—see page Primary Aldosteronism). These syndromes frequently have overlapping features. Hyperfunction may be compensatory, as in congenital adrenal hyperplasia (see page Overview of Congenital Adrenal Hyperplasia), or due to acquired hyperplasia, adenomas, or adenocarcinomas. Excess quantities of epinephrine and norepinephrine are produced in pheochromocytoma (see page Pheochromocytoma).

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