Endocrine Metabolism I: Introduction
depend heavily on trophic stimulation by anterior pituitary
hormones; therefore, although these peripheral endocrine
tissues are anatomically and functionally separated from
the central nervous system, they are indirectly dependent
on the hypothalamus and, thus, on the nervous system.
They produce low-molecular-weight hormones (steroids,
iodinated amines) having long-term effects that involve
regulation of gene expression.
The hierarchical organization of the endocrine system
emphasizes the substantial influence of the nervous sys-
tem on endocrine function; however, the influence of the
central nervous system is not always obligatory. Thus, al-
though C-cells and gut cells are of neuroblastic origin,
they function well in the absence of neural input; simi-
larly, the neural influence on hormone release from pan-
creatic islets and parathyroid glands is relatively unimpor-
tant. Nevertheless, the hypothalamus and adrenal medulla
fail when their neural connections are severed, leading
to atrophy of the anterior pituitary, adrenal cortex, thy-
roid, and gonads. However, two hormones are produced
by these tissues in normal or elevated amounts following
neural disconnection: prolactin from the anterior pituitary,
and aldosterone from the adrenal cortex. Release of aldos-
terone is regulated by the renin-angiotensin system and
by extracellular potassium levels, while that of prolactin
normally is under tonic inhibition by the hypothalamus
(Chapter 31).
A unidirectional scheme of endocrine control has been
alluded to above in the discussion of three levels of en-
docrine tissues: the nervous system-hypothalamus con-
trols the anterior pituitary, which in turn controls the
peripheral endocrine tissues. Closer examination of how
hormonal secretions are regulated reveals that, in many
instances, a closed-loop feedback (servo-mechanism) cir-
cuit operates to ensure that the correct amount of hormone
is released at any given time. In its simplest form, a cir-
cuit involves an endocrine cell that can monitor changes
in the blood level of the substance it regulates. This sens-
ing ability is coupled to a discriminator with an imprinted
“set point” such that if the circulating level deviates sig-
nificantly from the set point, the hormonal output is appro-
priately modified to counteract that deviation. This type of
negative feedback
regulation of hormone release—
usually involving one endocrine tissue, one hormone, and
one substance that is monitored—is the primary means
by which secretion of insulin, glucagon, parathyroid hor-
mone, and (to some extent) aldosterone is regulated
(Figure 30-13).
Another way in which hormonal secretion is regulated
involves a
neuroendocrine reflex,
which differs from a
neural reflex
in that the efferent neuron is replaced by a
F I G U R E 3 0 - 1 3
Simple negative feedback control of hormone release.
(Top) A
discriminator associated with an endocrine cell is capable of monitoring
blood levels of a regulated substance. If the level of the substance deviates
from the “set point,” the endocrine cell adjusts its hormonal output to
restore that level. The hormone may act either on the source of the
substance or on its removal.
(M iddle)
If the blood level of glucose rises
above the set point imprinted in the
cell of the pancreatic islet, insulin
secretion is increased. Insulin acts on the liver (source of glucose) to inhibit
(©) further production of glucose, thereby diminishing the input of
glucose into the blood glucose pool (broken line). Insulin also acts on
several tissues (muscle, others) to promote (©) glucose utilization, thereby
facilitating the removal of glucose from the blood glucose pool (solid line).
(Bottom )
Plasma K+ concentration is monitored by the zona glomerulosa
of the adrenal cortex, and an elevation will stimulate the release of
aldosterone. Aldosterone acts only on the disposal of K+, thereby serving
to control the level of K+ in blood. ECF, Extracellular fluid.
neuroendocrine cell (Table 30-5). As in a neural reflex arc,
a sensory (afferent) neuron conveys, via synaptic connec-
tions, signals emitted from a sensory receptor to an effer-
ent (neuroendocrine) cell, feedback which then affects the
function of an effector organ or tissue. Release of oxytocin,
ADH (vasopressin), and adrenal medullary hormones is
regulated in this way (Table 30-5). No direct negative feed-
back comparable to that in the previous model operates;
however, the efferent signal (hormone) counteracts, alle-
viates, or compensates for the stimulus that initiated the
reflex. Several examples follow. By increasing water re-
absorption, ADH promotes osmodilution and volume ex-
pansion, which counteract the dehydration that triggered
distress signals from osmoreceptors and baroreceptors; by
causing milk ejection, oxytocin helps appease the suckling
infant. The adrenal medullary catecholamines produce
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