The adrenal medulla functions as part of the autonomic nervous system. Stimulation of preganglionic sympathetic nerve fibers, which travel directly to the cells of the adrenal medulla, causes re-lease of the catecholamine hormones epinephrine and norepi-nephrine. About 90% of the secretion of the human adrenal medulla is epinephrine (also called adrenaline). Catecholamines regulate metabolic pathways to promote catabolism of stored fuels to meet caloric needs from endogenous sources. The major effects of epinephrine release are to prepare to meet a challenge (fight-or-flight response). Secretion of epinephrine causes de-creased blood flow to tissues that are not needed in emergency sit-uations, such as the gastrointestinal tract, and causes increased blood flow to tissues that are important for effective fight or flight, such as cardiac and skeletal muscle. Catecholamines also induce the release of free fatty acids, increase the basal metabolic rate, and elevate the blood glucose level.
A functioning adrenal cortex is necessary for life; adrenocortical secretions make it possible for the body to adapt to stress of all kinds. The three types of steroid hormones produced by the adrenal cortex are glucocorticoids, the prototype of which is hydrocortisone; mineralocorticoids, mainly aldosterone; and sex hormones, mainly androgens (male sex hormones). Without the adrenal cortex, severe stress would cause peripheral circulatory failure, circulatory shock, and prostration. Survival in the absence of a functioning adrenal cortex is possible only with nutritional, electrolyte, and fluid replacement and appropriate replacement with exogenous adrenocortical hormones.
The glucocorticoids are so named because they have an im-portant influence on glucose metabolism: increased hydro-cortisone secretion results in elevated blood glucose levels. However, the glucocorticoids have major effects on the me-tabolism of almost all organs of the body. Glucocorticoids are secreted from the adrenal cortex in response to the release of ACTH from the anterior lobe of the pituitary gland. This system represents an example of negative feedback. The pres-ence of glucocorticoids in the blood inhibits the release of corticotropin-releasing factor from the hypothalamus and also in-hibits ACTH secretion from the pituitary. The resultant decrease in ACTH secretion causes diminished release of glu-cocorticoids from the adrenal cortex.
Glucocorticoids (in the form of corticosteroids) are admin-istered frequently to inhibit the inflammatory response to tis-sue injury and suppress allergic manifestations. Their side effects include the development of diabetes mellitus, osteo-porosis, peptic ulcer, increased protein breakdown resulting in muscle wasting and poor wound healing, and redistribution of body fat.
Large amounts of exogenously administered glucocorticoids in the blood inhibit the release of ACTH and endogenous glu-cocorticoids. Because of this, the adrenal cortex can atrophy. If exogenous glucocorticoid administration is discontinued sud-denly, adrenal insufficiency results because of the inability of the atrophied cortex to respond adequately.
Mineralocorticoids exert their major effects on electrolyte me-tabolism. They act principally on the renal tubular and gas-trointestinal epithelium to cause increased sodium ion absorption in exchange for excretion of potassium or hydrogen ions. ACTH only minimally influences aldosterone secretion. It is primarily secreted in response to the presence of angiotensin II in the bloodstream. Angiotensin II is a substance that elevates the blood pressure by constricting arterioles. Its concentration is in-creased when renin is released from the kidney in response to de-creased perfusion pressure. The resultant increased aldosterone levels promote sodium reabsorption by the kidney and the gastrointestinal tract, which tends to restore blood pressure to normal. The release of aldosterone is also increased by hyper-kalemia. Aldosterone is the primary hormone for the long-term regulation of sodium balance.
Androgens, the third major type of steroid hormones produced by the adrenal cortex, exert effects similar to those of male sex hormones. The adrenal gland may also secrete small amounts of some estrogens, or female sex hormones. ACTH controls the se-cretion of adrenal androgens. When secreted in normal amounts, the adrenal androgens probably have little effect, but when se-creted in excess, in certain inborn enzyme deficiencies, masculin-ization may result. This is termed the adrenogenital syndrome.
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