книги студ / color atlas of physiology 5th ed[1]. (a. despopoulos et al, thieme 2003)

Organization of the Autonomic

Nervous System

In the somatic nervous system, nerve fibers extend to and from the skeletal muscles, skin and sense organs. They usually emit impulses in response to stimuli from the outside environment, as in the withdrawal reflex (!p. 320). Much somatic nervous activity occurs consciously and under voluntary control. In contrast, the autonomic nervous system (ANS) is mainly concerned with regulation of circulation and internal organs. It responds to changing outside conditions by triggering orthostatic responses, work start reactions, etc. to regulate the body’s internal environment

(!p. 2). As the name implies, most activities of the ANS are not subject to voluntary control.

For the most part, the autonomic and somatic nervous systems are anatomically and functionally separate in the periphery (!A), but closely connected in the central nervous system, CNS (!p. 266). The peripheral ANS is efferent, but most of the nerves containing ANS fibers hold also afferent neurons. These are called visceral afferents because their signals originate from visceral organs, such as the esophagus, gastrointestinal (GI) tract, liver, lungs, heart, arteries, and urinary bladder. Some are also named after the nerve they accompany (e.g., vagal afferents).

Autonomic nervous activity is usually regulated by the reflex arc, which has an afferent limb (visceral and/or somatic afferents) and an efferent limb (autonomic and/or somatic efferents). The afferent fibers convey stimuli from the skin (e.g. nociceptive stimuli; !p. 316) and nocisensors, mechanosensors and chemosensors in organs such as the lungs, gastrointestinal tract, bladder, vascular system and genitals. The ANS provides the autonomic efferent fibers that convey the reflex response to such afferent information, thereby inducing smooth muscle contraction (!p. 70) in organs such as the eye, lung, digestive tract and bladder, and influencing the function of the heart (!p. 194) and glands. Examples of somatic nervous system involvement are afferent

78stimuli from the skin and sense organs (e.g., light stimuli) and efferent impulses to the skeletal muscles (e.g., coughing and vomiting).

Simple reflexes can take place within an organ (e.g., in the gut, !p. 244), but complex reflexes are controlled by superordinate autonomic centers in the CNS, primarily in the spinal cord (!A). These centers are controlled by the hypothalamus, which incorporates the ANS in the execution of its programs (!p. 330). The cerebral cortex is an even higher-ranking center that integrates the ANS with other systems.

The peripheral ANS consists of a sympathetic division and a parasympathetic division (!A) which, for the most part, are separate entities (!also p. 80ff.). The autonomic centers of the sympathetic division lie in the thoracic and lumbar levels of the spinal cord, and those of the parasympathetic division lie in the brain stem (eyes, glands, and organs innervated by the vagus nerve) and sacral part of the spinal cord (bladder, lower parts of the large intestine, and genital organs). (!A). Preganglionic fibers of both divisions of the ANS extend from their centers to the ganglia, where they terminate at the postganglionic neurons.

Preganglionic sympathetic neurons arising from the spinal cord terminate either in the paravertebral ganglionic chain, in the cervical or abdominal ganglia or in so-called terminal ganglia. Transmission of stimuli from preganglionic to postganglionic neurons is cholinergic, that is, mediated by release of the neurotransmitter acetylcholine (!p. 82). Stimulation of all effector organs except sweat glands by the postganglionic sympathetic fibers is adrenergic, i.e., mediated by the release of norepinephrine (!A and p. 84ff.).

Parasympathetic ganglia are situated near or within the effector organ. Synaptic transmissions in the parasympathetic ganglia and at the effector organ are cholinergic (!A).

Most organs are innervated by sympathetic and parasympathetic nerve fibers. Nonetheless, the organ’s response to the two systems can be either antagonistic (e.g., in the heart) or complementary (e.g., in the sex organs).

The adrenal medulla is a ganglion and hormone gland combined. Preganglionic sympathetic fibers in the adrenal medulla release acetylcholine, leading to the secretion of epinephrine (and some norepinephrine) into the bloodstream (!p. 86).

Plate 3.1 Organization of ANS

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3 Autonomic Nervous System (ANS)

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A. Functions of the autonomic nervous system (ANS)

Plate 3.2 u. 3.3 Functions of ANS

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3 Autonomic Nervous System (ANS)

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tein kinase A (PKA), which phosphorylates different proteins, depending on the target cell type (!p. 274).

NE and E work via "1-adrenoceptors (!B3) to open L-type Ca2+ channels in cardiac cell membranes. This increases the [Ca2+]i and therefore produces positive chronotropic, dromotropic, and inotropic effects. Activated Gs protein can also directly increase the open-

probability of voltage-gated Ca2+ channels in the heart. In the kidney, the basal renin secretion is increased via !1-adrenoceptors.

3 Autonomic Nervous System (ANS)

!

gastrointestinal tract. Further effects of !2- adrenoceptor activation are increased insulin secretion and glycogenolysis in liver and muscle and decreased platelet aggregation. Epinephrine also enhances NE release in noradrenergic fibers by way of presynaptic !2- adrenoceptors (!A2, A5).

Heat production is increased via !3-adreno- ceptors on brown lipocytes (!p. 222).

NE in the synaptic cleft is deactivated by

(!A6 a – d):

diffusion of NE from the synaptic cleft into the blood;

extraneuronal NE uptake (in the heart, glands, smooth muscles, glia, and liver), and subsequent intracellular degradation of NE by catecholamine-O-methyltransferase (COMT) and monoamine oxidase (MAO);

active re-uptake of NE (70%) by the presynaptic nerve terminal. Some of the absorbed NE enters intracellular vesicles (!A3) and is reused, and some is inactivated by MAO;

stimulation of presynaptic α2-adrenocep- tors (autoreceptors; !A 6d, 7) by NE in the synaptic cleft, which inhibits the further release of NE.

Presynaptic α2-adrenoceptors can also be found on cholinergic nerve endings, e.g., in the gastrointestinal tract (motility") and cardiac atrium (negative dromotropic effect), whereas presynaptic M-cholinoceptors are present on noradrenergic nerve terminals. Their mutual interaction permits a certain degree of peripheral ANS regulation.

In alarm reactions, secretion of E (and some NE) from the adrenal medulla increases substantially in response to physical and mental or emotional stress. Therefore, cells not sympathetically innervated are also activated in such stress reactions. E also increases neuronal NE release via presynaptic !2-adrenoceptors (!A2). Epinephrine secretion from the adrenal medulla (mediated by increased sympathetic activity) is stimulated by certain triggers, e.g., physical work, cold, heat, anxiety, anger (stress), pain, oxygen deficiency, or a drop in blood pressure. In severe hypoglycemia (!30 mg/dL), for example, the plasma epinephrine concentration can increase by as much as 20-fold, while the norepinephrine concentration increases by a factor of only 2.5, resulting in a corresponding rise in the E/NE ratio.

The main task of epinephrine is to mobilize stored chemical energy, e.g., through lipolysis and glycogenolysis. Epinephrine enhances the uptake of glucose into skeletal muscle (!p. 282) and activates enzymes that accelerate glycolysis and lactate formation (!p. 72ff.). To enhance the blood flow in the muscles involved, the body increases the cardiac output while curbing gastrointestinal blood flow and activity (!p. 75 A). Adrenal epinephrine and neuronal NE begin to stimulate the secretion of hormones responsible for replenishing the depleted energy reserves (e.g., ACTH; !p. 297 A) while the alarm reaction is still in process.

Non-cholinergic, Non-adrenergic

Transmitters

In humans, gastrin-releasing peptide (GRP) and vasoactive intestinal peptide (VIP) serve as co-transmitters in preganglionic sympathetic fibers; neuropeptide Y (NPY) and somatostatin (SIH) are the ones involved in postganglionic fibers. Postganglionic parasympathetic fibers utilize the peptides enkephalin, substance P (SP) and/or NPY as co-transmitters.

Modulation of postsynaptic neurons seems to be the primary goal of preganglionic peptide secretion. There is substantial evidence demonstrating that ATP (adenosine triphosphate), NPY and VIP also function as independent neu-

!

rotransmitters in the autonomic nervous system. VIP and acetylcholine often occur jointly (but in separate vesicles) in the parasympathetic fibers of blood vessels, exocrine glands, and sweat glands. Within the gastrointestinal tract, VIP (along with nitric oxide) induces the slackening of the circular muscle layer and sphincter muscles and (with the co-transmit- ters dynorphin and galanin) enhances intesti-

nal secretion. Nitric oxide (NO) is liberated from nitrergic neurons (!p. 278)

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