section 30.6
Organization of the Endocrine System
725
T A B L E 3 0 -5
Neuroendocrine Reflex
S e n s o r y
re c e p to r
S e n s o r y n eu ro n
N e u r o e n d o c r in e c e ll
H o rm o n e
E ffecto r c e ll
Sensory Receptor
Sensory Neuron
Neuroendocrine
Cell
Hormone
Effector; Effects
Cardiovascular
Cranial nerves IX
Magnocellular
ADH
Kidney; water
baroreceptors
and X
neurons, hypothalamic
reabsorption
Osmoreceptors
? Osmoreceptor
PVN*, SON+
(As above)
(As above)
(As above)
Touch receptors
neuron
Ascending touch
(As above)
Oxytocin
Mammary gland;
in nipple
Uterine stretch
pathways
Unclear
(As above)
(As above)
milk ejection
Uterus; smooth muscle
receptors
Various receptors
Many
Adrenal medulla
Epinephrine,
contraction
Cardiovascular
of noxious stimuli
norepinephrine
augmentation and
liberation of energy
substrates
*PVN = paraventricular nucleus.
fSON = supraoptic nucleus.
cardiovascular and metabolic changes that enable the in-
dividual to cope with the stressful situation that triggered
their release, while the adrenal medullary enkephalins
probably serve to suppress the sensation of traumatic pain.
The neuroendocrine reflex is usually polysynaptic, i.e., one
or more interneurons connect the sensory neuron to the en-
docrine cell. Thus, the system is more amenable to modu-
lation by other neurons or hormones, serving to fine-tune
the system. For example, under conditions of normal extra-
cellular fluid volume and osmolality (i.e., when ADH re-
lease is suppressed), the sensation of pain stimulates the re-
lease of ADH and promotes water retention. Pain-induced
release of ADH may be due to neural discharge of endor-
phins or enkephalins in the central nervous system, which
act on the hypothalamus. The peripheral hormones (level
III, Figure 30-12) also influence the neuroendocrine re-
flex. Cortisol, for example, amplifies the adrenal medullary
response to stress by increasing the excitability of in-
terneurons in the reticular formation and by stimulating
the synthesis of adrenal medullary phenylethanolamine
N-methyltransferase (PNMT), which catalyzes the forma-
tion of epinephrine (Chapter 32). Estrogen is an impor-
tant regulator of hypothalamic pro-oxyphysin synthesis
(Chapter
31)
and
thus
promotes
the
formation
of
oxytocin.
Some hormones are under complex
feedback regula-
tion
involving both a neuroendocrine reflex and a nega-
tive feedback circuit. Invariably, the neuroendocrine re-
flex component involves the hypothalamus, which in one
instance is also the site of positive feedback (Chapter 34).
The “substance” that is monitored and exerts negative
feedback may be a substrate (e.g., glucose, amino acid)
or the hormone that is being regulated. Generally, two
or more hormones are involved, which is not surpris-
ing, since most hypothalamic and anterior pituitary hor-
mones subserve the function of regulating the release of
another hormone (Figure 30-14). As examples, release
of growth hormone is regulated by growth hormone-
releasing hormone and somatostatin; that of prolactin
by prolactin-releasing factor and prolactin-inhibiting fac-
tor (dopamine); that of thyroid hormone by thyrotropin-
releasing hormone and thyroid-stimulating hormone; that
of cortisol by corticotropin-releasing hormone and corti-
cotropin; and that of the sex steroids by gonadotropin-
releasing hormone, luteinizing hormone, and follicle-
stimulating hormone.
