Page 99 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

!
gastrointestinal tract. Further effects of ! 2- In alarm reactions, secretion of E (and some
adrenoceptor activation are increased insulin NE) from the adrenal medulla increases sub-
secretion and glycogenolysis in liver and stantially in response to physical and mental or
muscle and decreased platelet aggregation. Epi- emotional stress. Therefore, cells not sympa-
nephrine also enhances NE release in nor- thetically innervated are also activated in such
adrenergic fibers by way of presynaptic ! 2- stress reactions. E also increases neuronal NE
adrenoceptors (! A2, A5). release via presynaptic ! 2-adrenoceptors
Heat production is increased via ! 3-adreno- (! A2). Epinephrine secretion from the
adrenal medulla (mediated by increased sym-
ceptors on brown lipocytes (! p. 222).
Autonomic Nervous System (ANS) the blood; (COMT) anger (stress), pain, oxygen deficiency, or a drop
pathetic activity) is stimulated by certain trig-
NE in the synaptic cleft is deactivated by
gers, e.g., physical work, cold, heat, anxiety,
(! A6 a – d):
! diffusion of NE from the synaptic cleft into
in blood pressure. In severe hypoglycemia
(! 30 mg/dL), for example, the plasma epi-
! extraneuronal NE uptake (in the heart,
nephrine concentration can increase by as
glands, smooth muscles, glia, and liver), and
much as 20-fold, while the norepinephrine
subsequent intracellular degradation of NE by
concentration increases by a factor of only 2.5,
catecholamine-O-methyltransferase
and monoamine oxidase (MAO);
resulting in a corresponding rise in the E/NE
ratio.
! active re-uptake of NE (70%) by the presyn-
The main task of epinephrine is to mobilize
enters intracellular vesicles (! A3) and is re-
used, and some is inactivated by MAO;
and glycogenolysis. Epinephrine enhances the
3 aptic nerve terminal. Some of the absorbed NE stored chemical energy, e.g., through lipolysis
of
! stimulation of presynaptic α 2-adrenocep-
muscle
skeletal
glucose into
uptake
tors (autoreceptors; ! A 6d, 7) by NE in the (! p. 282) and activates enzymes that accel-
synaptic cleft, which inhibits the further re- erate glycolysis and lactate formation
lease of NE. (! p. 72ff.). To enhance the blood flow in the
Presynaptic α 2-adrenoceptors can also be muscles involved, the body increases the car-
found on cholinergic nerve endings, e.g., in the diac output while curbing gastrointestinal
gastrointestinal tract (motility") and cardiac blood flow and activity (! p. 75 A). Adrenal ep-
atrium (negative dromotropic effect), whereas inephrine and neuronal NE begin to stimulate
presynaptic M-cholinoceptors are present on the secretion of hormones responsible for re-
noradrenergic nerve terminals. Their mutual plenishing the depleted energy reserves (e.g.,
interaction permits a certain degree of periph- ACTH; ! p. 297 A) while the alarm reaction is
eral ANS regulation. still in process.
Adrenal Medulla Non-cholinergic, Non-adrenergic
Transmitters
After stimulation of preganglionic sympa-
thetic nerve fibers (cholinergic transmission; In humans, gastrin-releasing peptide (GRP)
! p. 81), 95% of all cells in the adrenal medulla and vasoactive intestinal peptide (VIP) serve as
secrete the endocrine hormone epinephrine co-transmitters in preganglionic sympathetic
(E) into the blood by exocytosis, and another fibers; neuropeptide Y (NPY) and somatostatin
5% release norepinephrine (NE). Compared to (SIH) are the ones involved in postganglionic
noradrenergic neurons (see above), NE synthe- fibers. Postganglionic parasympathetic fibers
sis in the adrenal medulla is similar, but most utilize the peptides enkephalin, substance P
of the NE leaves the vesicle and is enzymati- (SP) and/or NPY as co-transmitters.
cally metabolized into E in the cytoplasm. Modulation of postsynaptic neurons seems
Special vesicles called chromaffin bodies then to be the primary goal of preganglionic peptide
actively store E and get ready to release it and secretion. There is substantial evidence dem-
co-transmitters (enkephalin, neuropeptide Y) onstrating that ATP (adenosine triphosphate),
86 by exocytosis. NPY and VIP also function as independent neu-
!
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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