Page 285 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Therapeutic administration of a hormone (e.g.,
Humoral Signals: Control and Effects cortisone, a cortisol substitute) have the same effect
on higher hormone secretion (ACTH and CRH in the
Hormones and other humoral signals function example) as that of the end-hormone (cortisol in the
to provide feedback control, a mechanism in example) normally secreted by the peripheral gland
which the response to a signal feeds back on (adrenal cortex in this case). Long-term administra-
the signal generator (e.g., endocrine gland). tion of an end-hormone would therefore lead to in-
The speed at which control measures are im- hibition and atrophy of the endocrine gland or cells
plemented depends on the rate at which the that normally produce that hormone. This is known
signal substance is broken down—the quicker as compensatory atrophy.
the degradation process, the faster and more A rebound effect can occur if secretion of the
Hormones and Reproduction nal. In the example shown in A1, a rise in mone administration.
flexible the control.
higher hormone (e.g., ACTH) is temporarily
In negative feedback control, the response
elevated after discontinuation of end-hor-
to a feedback signal opposes the original sig-
The principal functions of endocrine hor-
plasma cortisol in response to the release of
mones, paracrine hormones and other humoral
hor-
corticoliberin
(corticotropin-releasing
transmitter substances are to control and
mone, CRH) from the hypothalamus leads to
regulate:
down-regulation of the signal cascade “CRH !
! enzyme activity by altering the conforma-
ACTH ! adrenal cortex,” resulting in a
synthesis of the enzyme (induction);
back loops, ACTH can also negatively feed back
! transport processes, e.g., by changing the
on the hypothalamus ( ! A2), and cortisol, the
rate of insertion and synthesis of ion channels/
11 decrease in cortisol secretion. In shorter feed- tion (allosterism) or inhibiting/stimulating the
end-hormone, can negatively feed back on the carriers or by changing their opening probabil-
anterior pituitary (! A3). In some cases, the ity or affinity;
metabolic parameter regulated by a hormone ! growth (see above), i.e., increasing the rate
(e.g., plasma glucose concentration) rather of mitosis (proliferation), “programmed cell
then the hormone itself represents the feed- death” (apoptosis) or through cell differentia-
back signal. In the example (! B), glucagon in- tion or dedifferentiation;
creases blood glucose levels (while insulin ! secretion of other hormones. Regulation can
decreases them), which in turn inhibits the occur via endocrine pathways (e.g., ACTH-me-
secretion of glucagon (and stimulates that of diated cortisol secretion; ! A5), a short portal
insulin). Neuronal signals can also serve as vein-like circuit within the organ (e.g., effect of
feedback (neuroendocrine feedback) used, for CRH on ACTH secretion, ! A4), or the effect of
example, to regulate plasma osmolality cortisol from the adrenal cortex on the synthe-
(! p. 170). sis of epinephrine in the adrenal medulla,
In positive feedback control, the response to (! A6), or via paracrine pathways (e.g., the ef-
the feedback amplifies the original signal and fect of somatostatin, SIH, on the secretion of
heightens the overall response (e.g., in auto- insulin and glucagon; ! B).
crine regulation; see below). Cells that have receptors for their own
The higher hormone not only controls the humoral signals transmit autocrine signals
synthesis and excretion of the end-hormone, that function to
but also controls the growth of peripheral en- ! exert negative feedback control on a target
docrine gland. If, for example, the end-hor- cell, e.g., to discontinue secretion of a trans-
mone concentration in the blood is too low mitter (e.g., norepinephrine; ! p. 84);
despite maximum synthesis and secretion of ! coordinate cells of the same type (e.g., in
the existing endocrine cells, the gland will en- growth);
large to increase end-hormone production. ! exert positive feedback control on the secret-
This type of compensatory hypertrophy is ob- ing cell or to cells of the same type. These
served for instance in goiter development mechanisms serve to amplify weak signals as
(! p. 288) and can also occur after surgical ex- is observed in the eicosanoid secretion or in T
272
cision of part of the gland. cell clonal expansion (! p. 96ff.).
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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