cf >> L'ipercorticosurrenalismo
The adrenal glands are located at the upper pole of each kidney and are composed
of two distinct regions:
- the cortical
-the medullary.
The adrenal cortex consists, in turn, of three anatomical zones:
- the glomerular zone, the most external, which secretes aldosterone,
mineralocorticoid hormone;
- the fasciculata zone, intermediate area that secretes cortisol;
- the reticular zone, the innermost, which secretes adrenal androgens.
In particular we will have that: Glomerular zone, is made up of parenchymal
cells that synthesize and secrete mineralocorticoid hormones for the maintenance
of water balance
The glomerular area owes its name to the particular organization of the
glandular tissue in cellular cords wrapped around themselves to form rounded
structures ("glomeruli"). It produces mineralocorticoids, particularly
aldosterone, which increases sodium reabsorption in the distal tubule and in the
collecting duct; it also increases the elimination of potassium and hydrogenions.
As a consequence of sodium reabsorption there is an increase in the circulating
blood volume with an increase in arterial pressure.
Fasciculata zone, instead, synthesizes and secretes glucocorticoids and controls
the metabolism of carbohydrates, fats and proteins)
The fasciculated area is the intermediate layer between the layers of the
adrenal cortex, located between the glomerular area and the reticulated area. It
deals with synthesizing and secreting glucocorticoids and a small amount of
androgens (dehydroepiandrosterone or DHEAS). The tumor in the fasciculated area
may lead to a primary hypersecretion of the adrenal cortex.
Reticulated zone (produces sex hormones such as androgens, estrogens and
progesterone).
The adrenal medulla, located at the center of the gland, is, from the functional
point of view, connected to the sympathetic nervous system and secretes
catecholamines, epinephrine and norepinephrine, in response to stress. The
synthesis of all steroid hormones originates from cholesterol and is catalyzed
by a series of regulated enzymatic reactions. Glucocorticoids influence
metabolic processes, cardiovascular function, behavior and inflammatory / immune
response.
Cortisol, the human natural glucocorticoid, is secreted by the
adrenals in response to ultradian, circadian and stress-induced hormone
stimulation, mediated by the adrenocorticotropic hormone (adrenocorticotropic
hormone, ACTH). Plasma cortisol has a well-marked circadian rhythm, with higher
concentrations in the morning. ACTH, a neuropeptide of 39 amino acids, is part
of a molecular precursor, pro-opio-melanocortin (POMC), which also contains (beta-endorphin,
beta-lipotropin, the peptide-like corticotropin of the intermediate lobe (
corticotropin-like intermediate-lobe peptide, CLIP) and several
melanocyte-stimulating hormones (melanocyte-stimulating hormones, MSH) The
secretion of ACTH by the pituitary is regulated mainly by two hypothalamic
polypeptides: the corticotropin-releasing hormone ( corti-cotropin-releasing
hormone, CRH), a polypeptide of 41 amino acids, and vasopressin, a decapeptide.The
glucocorticoids exert a negative feedback on the secretion of CRH and ACTH.The
hypothalamic-pituitary-adrenal axis (hypothalamic-pituitary-adrenal) , HPA)
interacts and influences reproductive function, growth and thyroid function at
various levels, with increased participation of glucocorticoids at all levels.
They maintain metabolic homeostasis, regulate glycemia, have permissive effects
on gluconeogenesis (see carbohydrates), increase glycogen synthesis, induce an
increase in insulin levels, have permissive effects on lipolytic hormones,
increase catabolism, reduce anabolism ( except that of fats), inhibit the growth
hormone axis, inhibit the reproductive axis and also present mineralocorticoid
cortisol activity.
Influencing connective tissues, causing loss of collagen and connective tissue
Influencing calcium homeostasis. Stimulate osteoclasts, inhibit osteoblasts,
reduce intestinal absorption of calcium, stimulate parathyroid hormone release,
increase urinary calcium excretion, reduce phosphate resorption Maintain
cardiovascular function Increase cardiac output, increase vascular tone, have
permissive effects on pressure hormones, increase sodium retention.
Influencing behavior and cognitive function Influencing the immune system
Increase intravascular concentration of leukocytes, reduce the migration of
inflammatory cells to the sites of damage, suppress the immune system (thymolysis,
suppression of cytokines, prostanoids, quinins, serotonin, histamine,
collagenase and plasminogen activator).
The renin-angiotensin-aldosterone system is the most important control factor in
the secretion of aldosterone. The juxtaglomerular cells of the kidney secrete
renin in response to the decrease in circulating volume and / or the reduction
of renal perfusion pressure. Renin is the speed-limiting enzyme that splits the
angiotensinogen angiotensinogen of 60 kDa, synthesized by the liver, into the
bioinactive angiotensin decapeptide I. This is rapidly converted into the
octapeptide angiotensin II by the angiotensin-converting enzyme (angiotensin-converting
enzyme, ACE) in the lungs and other tissues. Angiotensin II is a potent
vasoconstrictor and also stimulates the production of aldosterone, but not that
of cortisol. It is the predominant regulator of aldosterone secretion, but this
is also influenced by plasma potassium, sodium balance and ACTH. ACTH averages
probably the circadian rhythm of aldosterone, determining its morning
concentration peaks. Aldosterone binds to mineralocorticoid type I receptors,
while cortisol binds to type II glucocorticoid receptors. The binding of
aldosterone to mineralocorticoid receptors of the renal cytosol induces the
outflow of Na + into the extracellular fluid and the secretion of K + and H +
through the sodium-potassium pump. The consequent increase in sodium and the
decrease in plasma potassium induce a feedback mechanism to suppress renin
secretion and, consequently, that of aldosterone. About 5% of cortisol and 40%
of aldosterone are in unbound form. The remainder is bound to
corticosteroid-binding globulin and albumin. Adrenal androgens include
dehydroepiandrosterone (DHEA), its sulfated form (DHEAS) and androstenedione.
These are synthesized in the reticular zone under the influence of ACTH and
other factors stimulating adrenal androgens. Although adrenal androgens have
minimal intrinsic androgenic activity, they contribute to androgenicity through
their peripheral conversion to testosterone and dihydrotestosterone. In adult
males, an excess of adrenal androgens has no clinical consequences; in females,
however, the peripheral conversion of excessive quantities of adrenal androgens
causes acne, hirsutism and virilization. Because of the gonadal production of
androgens and estrogens and of norepinephrine secretion by sympathetic ganglia,
the lack of androgens and adrenal catecholamines is not clinically evident.