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1. pertaining to one of the small glands just above each kidney. Called also suprarenal.
adrenal gland a small triangular endocrine gland situated in the retroperitoneal tissues at the cranial pole of each kidney; it is the result of fusion of two organs, one forming the inner core or medulla, and the other forming an outer shell, or cortex. These two structures are different in both their anatomy and the kinds of hormone they synthesize and secrete. Called also suprarenal gland.
Adrenal glands.
Adrenal Medulla. This is actually a glandular extension of sympathetic effector fibers or postganglionic neurons. It releases the hormones epinephrine and norepinephrine in response to stimulation of the sympathetic nervous system. These hormones enter the blood stream and are carried throughout the body where they indirectly act as stimulants to the various organs. Their production and distribution by the blood usually occur at the same time that the organs are being stimulated by the sympathetic nerves. In this way, the adrenal medulla and the sympathetic nerves support each other and can act as substitutes for each other. Epinephrine and norepinephrine both constrict blood vessels (except in muscle tissue) and are released in anticipatory states and other times of increased emotion, causing such changes as elevated blood pressure; release of glucagon, insulin, and fatty acids into the blood; and increases in heart rate, sweating, metabolic rate, and peristaltic activity. Epinephrine is important in initiating the physiological changes in the “fight or flight” response (see alarm reaction) and has a more prolonged effect than norepinephrine because of being removed more slowly from the blood.
Adrenal Cortex. The adrenal cortex synthesizes and secretes more than 30 different steroids and is responsible for the maintenance of several life-sustaining physiological activities. The steroids are divided into three major groups: glucocorticoids, mineralocorticoids, and androgens. The glucocorticoids get their name from the fact that they cause an increase in blood glucose levels (gluco-), are produced by the adrenal cortex (corti-), and are synthesized from cholesterol, which is a steroid (-oid). The mineralocorticoids, as their name implies, are chiefly concerned with the concentration of electrolytes (minerals) in the extracellular fluid. The adrenal cortex also secretes small amounts of androgens and is the major source of these hormones in females.
Glucocorticoids. The principal glucocorticoid is cortisol (also known as hydrocortisone), which is responsible for more than 95 per cent of all glucocorticoid activity. The remainder of the hormonal activity is provided by corticosterone and cortisone.

The physiologic effects of the glucocorticoids promote the metabolic breakdown or anabolism of carbohydrates, proteins, and fats. Cortisol increases the rate of gluconeogenesis by the liver, decreases the utilization of glucose by the cells, reduces cellular protein and enhances utilization of amino acids by the liver, and promotes mobilization of fatty acids from adipose tissue into the plasma. The net effect of these actions is to make these noncarbohydrate nutritive elements readily available for energy.

The regulation of cortisol secretion involves a complex closed-loop negative feedback system. Initially, the hypothalamus reacts to physical or psychogenic stress by secreting corticotropin-releasing hormone (CRH), which is carried to the anterior pituitary gland (adenohypophysis) via the hypothalamic-hypophyseal portal system. In response to the presence of CRH, the adenohypophysis secretes adrenocorticotropic hormone (ACTH), which stimulates the adrenal cortex to release cortisol. Cortisol then initiates a series of metabolic activities which help to relieve the physiologic effects of stress. Cortisol inhibits both release of CRH from the hypothalamus and of ACTH from the adenohypophysis. This exerts a negative feedback effect; high serum cortisol levels inhibit further production of cortisol. Thus, during times of relative calm when the body is not experiencing abnormal stress, the cortisol level returns to normal.

Another factor that influences the secretory rates of CRH, ACTH, and cortisol is a biologic clock mechanism that establishes a cyclic pattern of signals from the hypothalamus. This is a 24-hour cycle that has its peak right after completion of the major portion of a night's sleep, usually around 4 or 5 AM. About 12 hours later, the blood level of cortisol is at its lowest. This cycle is dependent on sleeping patterns; therefore, if a person changes the pattern and sleeps in the daytime, the cycle of hormonal levels changes accordingly. This information is significant in testing for cortisol levels as a means of diagnosing a disorder of the endocrine system. When blood is drawn for testing, the specimen should be clearly labeled as to the precise time it was taken.
Mineralocorticoids. The principal mineralocorticoid is aldosterone. This and other mineralocorticoids prevent excessive loss of sodium and chloride in the urine by enhancing their reabsorption from the distal ends of the renal tubules. They have the same effect to a lesser degree on the sweat and salivary glands and on the intestines. Additionally, aldosterone promotes excretion of potassium in the urine. The net result of these activities is the maintenance of fluid and electrolyte balance in the blood and extracellular fluid, which, in turn, affects cardiac output and blood pressure. A deficit of aldosterone secretion brings about a decrease in extracellular fluid and blood volumes, interference with the venous return to the heart, and a fall in cardiac output. If not corrected, the patient rapidly goes into profound shock.
Dysfunction of the Adrenal Glands. Either increased levels or deficits of the adrenal hormones can produce various disorders. cushing's syndrome, called also primary aldosteronism, is related to excessive secretion of aldosterone. In addison's disease there is an overall hypofunction of the adrenal cortex, resulting in insufficient production of all three groups of adrenocortical hormones. adrenogenital syndrome, which is usually caused by a tumor of the adrenal cortex, results from excessive secretion of androgens. Since androgens have a masculinizing effect, the symptoms are primarily those of changes in the secondary sex characteristics.


1. Near or on the kidney; denoting the suprarenal (adrenal) gland.
2. A suprarenal gland or separate tissue or product thereof.

See also: suprarenal.
[L. ad, to, + ren, kidney]


/ad·re·nal/ (ah-dre´n'l)
3. pertaining to an adrenal gland.


1. At, near, or on the kidneys.
2. Of or relating to the adrenal glands or their secretions.
An adrenal gland.

ad·re′nal·ly adv.


Etymology: L, ad, to, ren, kidney
pertaining to the adrenal glands, which are located atop the kidneys. Also called suprarenal.


1. Near or on the kidney; denoting the suprarenal (adrenal) gland.
2. A suprarenal gland or separate tissue or product thereof.
See also: suprarenal
[L. ad, to, + ren, kidney]


Refers to the glands which sit on top of each kidney and that secrete various hormones.
Mentioned in: Hyperaldosteronism


1. near the kidney.
2. of or produced by the adrenal glands.
3. an adrenal gland.

adrenal cortex
the outer part of the adrenal gland made up of an external zona glomerulosa, a deeper zona fasciculata and a zona reticularis. It produces three main groups of hormones, the glucocorticoids which are concerned with increasing blood glucose levels, the mineralocorticoids concerned with the maintenance of electrolyte levels in the extracellular fluid, and androgens which have the same masculinizing effect as the hormone testosterone produced by the testis. Called also adrenal gland cortex. See glucocorticoid, mineralocorticoid, androgen.
adrenal cortex inhibitors
adrenal cortical dysfunction
adrenal function tests
see acth response test, dexamethasone suppression test, v-test.
adrenal hyperplasia-like syndrome
a congenital abnormality of adrenal steroidogenesis reported in dogs which results in hyperprogestinism and hyperandrogenism. Clinical signs include bilaterally symmetrical alopecia resembling that seen with other endocrinopathies.
adrenal insufficiency
hypofunction of the adrenal gland, particularly the cortex, leading to signs of weakness and loss of sodium, chloride and water. See also primary hypoadrenocorticism.
adrenal medulla
a glandular extension of the effector fibers of the sympathetic nervous system that releases into the bloodstream the hormones epinephrine (adrenaline) and norepinephrine (noradrenaline). When the sympathetic nervous system is stimulated the adrenal medulla responds also and its hormones are carried via the bloodstream to cause increases in cardiac output and metabolic rate, vasoconstriction and reduction of gastrointestinal peristalsis. The hormones have similar functions but epinephrine is removed from the bloodstream more slowly and has a more prolonged effect. Called also adrenal gland medulla.
Adrenal medullary hormones are not essential to life. Hypersecretion, such as occurs in some functional pheochromocytomas, causes tachycardia, edema and cardiac hypertrophy.
adrenal steroids
cortisol, corticosterone, cortisone, 11-dehydroxycortisone, desoxycorticosterone, 17-hydroxy-11-desoxycorticosterone, aldosterone, the adrenal corticoids from the adrenal cortex. Called also corticosteroids.