ADRENAL
FUNCTION
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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