Page 270 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

lease or effect results in the excretion of large
The Antidiuretic Hormone amounts of poorly concentrated urine and hy-
pertonic dehydration (see also p.122), leading
The antidiuretic hormone ([ADH] adiuretin, va- to cell shrinkage. Patients will be forced to
sopressin) is formed in the supraoptic and compensate for the renal loss of water by
paraventricular nuclei of the hypothalamus drinking large amounts (polydipsia). If the os-
and is transported to the posterior lobe of the moreceptors in the hypothalamus are de-
pituitary gland via the axons of the hormone- stroyed, ADH deficiency is accompanied by hy-
producing neurons. ADH causes the incorpora- podipsia, and the hypertonic dehydration is
tion, via V 2 -receptors and cAMP, of water chan- especially marked. In psychogenic polydipsia
nels into the luminal membrane and thus pro- ADH release is inhibited because of the excess
motes water reabsorption in the distal tubules water, and thus, contrary to primary ADH defi-
and in the collecting duct of the kidney. ADH ciency, the result will be hypotonic hyperhy-
also stimulates the tubular absorption of Na + dration.
and urea. A high ADH concentration also leads
to vasoconstriction (via V 1 -receptors and IP 3 ).
Stimuli for the release of ADH are extracel- Prolactin
lular hyperosmolarity (or cell shrinkage) and Prolactin (→ B) is formed in the anterior lobe of
Hormones vomiting, pain, stress, and (sexual) arousal. the pituitary gland. It stimulates growth and
a decreased filling of the two atria, as well as
differentiation of the mammary gland as well
ADH secretion is further stimulated by angio-
but not the basal, release of the gonadotropins
(e.g., nicotine, morphine, barbiturates). In-
9 tensin II, dopamine, and some drugs or toxins as milk production. It inhibits the pulsatile,
creased atrial distension as well as γ-aminobu- (luteinizing hormone [LH] and follicle-stimu-
tyric acid (GABA), alcohol, and exposure to lating hormone [FSH]; → p. 274). It also inhib-
cold have an inhibitory effect. its cellular glucose uptake and the cellular im-
ADH excess (→ A1) is often due to raised mune defenses.
ADH formation in the hypothalamus, for exam- Touching the nipple of a lactating woman
ple, by stress. Furthermore, ADH can be formed and estrogens promote the release of prolac-
ectopically in tumors (especially small-cell tin. Its release is also stimulated by thyroliber-
bronchial carcinoma), or by lung disease. It in (thyroid-releasing hormone [TRH]), endor-
leads to reduced water excretion (oliguria). phins, vasoactive intestinal peptide (VIP), oxy-
The resulting marked concentration of poorly tocin, and angiotensin II as well as by stress,
dissolved urinary constituents can lead to the non–rapid eye movement (NREM) sleep, or hy-
formation of urinary stones (urolithiasis). At poglycemia. Dopamine inhibits prolactin re-
the same time there will be a drop in extracel- lease. As prolactin increases dopamine metab-
lular osmolarity (hypotonic hyperhydration) olism in the hypothalamus, it inhibits its own
and cell swelling occurs. This is especially dan- release (negative feedback).
gerous if it leads to cerebral edema (→ p. 358). Excess prolactin (→ B) can be caused by hor-
ADH deficiency (→ A2) occurs if release is mone-producing tumors, or by administration
reduced, as in genetically determined central of antidopaminergic drugs. Renal and liver fail-
diabetes insipidus, in destruction of neurones, ure can also result in an excess of prolactin,
for example, by autoimmune disease, or other possibly via a lack of dopamine. Hypothyroid-
pituitary gland injury. Exogenous causes in- ism raises prolactin release via corresponding-
clude alcohol or exposure to cold. On the other ly increased TRH secretion. The effects of ex-
hand, ADH may fail to have an effect on the cess prolactin are milk flow (galactorrhea),
kidney, even if it is normally secreted, for ex- tendency toward hyperglycemia, and an inhi-
ample, because of defective water channels, or bition of gonadotropin release, accompanied
if the concentrating capacity of the kidney is by hypogonadism, amenorrhea, loss of libido,
+
otherwise impaired, as in K deficiency, Ca 2+ and impotence.
260 excess, or inflammation of the renal medulla
(renal diabetes insipidus). Decreased ADH re-
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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