Page 276 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Adrenocorticoid Hormones: Causes of Abnormal Release
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The glucocorticoids serve, in the first instance, usually too high for K balance. If hypovolemia
in the adaptation of metabolism, circulation, occurs, the resulting “intertwining” of the reg-
blood, immune system, etc. to stress, i.e., se- ulatory circuits for plasma volume and potas-
vere physical and psychological threat. The sium (→ p. 258) regularly leads to hypokale-
mineralocorticoids act on mineral and water mia. Even if blood volume is normal or in-
balance (for mechanism of action see p. 268) creased, renal perfusion may be impaired and
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by aiding in the renal retention of Na and the thus renin release increased in a number of re-
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elimination of K and other ions. nal diseases. If the pumping action of the heart
The release of glucocorticoids (e.g., cortisol) is reduced (→ p. 224), or in peripheral vasodila-
is regulated by ACTH from the pituitary gland, tion (e.g., in sepsis or liver failure; → p.118) the
which is, in turn, under the control of cortico- blood pressure can be maintained only by mas-
liberin (corticotropin-releasing hormone sive activation of the sympathetic system, re-
[CRH]) from the hypothalamus (→ A). The sulting in renal vasoconstriction, renin release,
most important stimulus for the release of and hyperaldosteronism. Another cause may
CRH, and thus of ACTH and cortisol, is stress. be an aldosterone-producing tumor in the
Other stimuli are epinephrine, ADH, hista- adrenal (Conn’s syndrome). Furthermore, a de-
Hormones and hypoglycemia (→ A1). The organism’s p. 212) may result in an increased mineralocor-
fect of 11β-hydroxysteroid dehydrogenase (→
mine, pyrogens, pain, fall in blood pressure,
diurnal rhythm also plays a role: release of cor-
ticoid effect. The enzyme is normally formed in
cortisol. This fits into the mineralocorticoid re-
then slowly falls during the day (→ A2). The
9 tisol is highest in the early morning hours and the target cells of aldosterone and inactivates
release is inhibited by morphine. ceptor and its mineralocorticoid action is nor-
An excess of glucocorticoids often has an mally stopped only by enzymatic inactivation.
iatrogenic cause (therapeutic administration Because its concentration in blood is more than
of glucocorticoids for immunosuppression; a hundred times higher than that of aldoste-
→ A4), but it can also be the result of a hor- rone, cortisol will cause a massive mineralo-
mone-producing tumor in the adrenal gland corticoid effect if 11β-hydroxysteroid dehydro-
or other organs (especially small-cell bron- genase is defective. In a rare genetic defect
chial carcinoma; → A3) (Cushing’s disease; (glucocorticoid remediable hyperaldosteron-
→ p. 268). The cause may be an excess stimula- ism), the expression of aldosterone producing
tion of the adrenal by ACTH (secondary Cush- enzymes is driven by an ACTH-sensitive pro-
ing syndromes, for example, due to a pituitary motor, leading to enhanced aldosterone pro-
tumor, other causes of CRH release, or ectopic duction, whenever ACTH is high. Treatment of
formation of ACTH or, rarely, of CRH). the patients with glucocorticoids suppresses
An important stimulus for the release of the ACTH release and thus hyperaldosteronism. In
mineralocorticoid aldosterone is angiotensin yet another rare genetic disease the mineralo-
II, which is formed in increased amounts via corticoid receptor is sensitive to progesterone,
the renin–angiotensin system when the renal leading to pseudohyperaldosteronism which
perfusion pressure is reduced (→ A5). Aldoste- exacerbates in pregnancy.
rone release is also stimulated by ADH, whose A deficiency of adrenal hormones (→ B) can
secretion is stimulated by angiotensin II. Aldo- be the consequence of adrenal insufficiency
sterone release is increased by hyperkalemia, (Addison’s disease;→ p. 270; e.g., in genetic de-
but decreased by dopamine and the atrial na- fects, autoimmune adrenal disease, tuberculo-
triuretic factor (ANF). sis, metastases, surgical removal) or of enzyme
A selective excess of mineralocorticoids in defects in adrenal hormone synthesis
the majority of cases occurs in the form of sec- (→ p. 264). In addition, there may be insuffi-
ondary hyperaldosteronism caused by in- cient stimulation by ACTH, as in damage to the
creased renin release. In hypovolemia (e.g in pituitary gland or hypothalamus. Aldosterone
266 dehydration) the increased release of aldoste- release can also be reduced as a result of hypo-
rone is adequate for controlling volume, but kalemia or decreased angiotensin II formation.
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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