ANS centers in the brain stem act as relay stations for control of activities initiated at higher levels of the brain, such as the hypothalamus and cerebrum.
Visceral sensory signals entering the autonomic ganglia, spinal cord, brain stem, or hypothalamus elicit reflex responses which control the activity of visceral organs.
D Efferent output
Efferent autonomic signals are transmitted to the body through two major subdivisions of the ANS, the SNS, and PNS. (see later discussion.)
II Physiology of the autonomic nervous system
A Neurotransmitters
Acetylcholine (ACh) and norepinephrine (NE) are the main neurotransmitters.
All preganglionic neurons are cholinergic in both the SNS and PNS nervous systems and secrete ACh.
Postganglionic neurons of the PNS are cholinergic, while most postganglionic SNS neurons are adrenergic and secrete NE.The adrenal gland functions like a modified sympathetic ganglion and when stimulated by presynaptic SNS fibers, releases NE and epinephrine (EPI) into the circulation to act on sites distant from the gland; therefore, there is no postganglionic neuron.Sweat glands in horses are mostly apocrine and open into hair follicles. These glands and the piloerector muscles are stimulated by circulating EPI that acts on adrenergic (β2) receptors.Eccrine sweat glands are common in humans, but are less common in horses. In humans, they constitute 90% of sweat glands and they are stimulated by a postganglionic SNS neuron that secretes ACh.
B Synthesis, duration of action, and degradation of ACh
ACh is synthesized within the axoplasm in the terminal endings of cholinergic nerves.
The ACh is transported to the interior of the vesicles where it is stored in a highly concentrated form until it is released along with ATP.
After release, ACh persists in the tissue for a few seconds, then most of it is split into an acetate ion and choline by the enzyme acetylcholinesterase, which is present in the terminal neuron and the surface of the receptor organ.
C Synthesis, duration of action, and removal of NE
Synthesis of norepinephrine from phenylalanine begins in the axoplasm of the terminal nerve endings of adrenergic nerve fibers and is completed inside the vesicles.
In the adrenal medulla, this reaction goes one step further and transforms about 85% of the norepinephrine into epinephrine.
After secretion, NE is rapidly (within a few seconds) removed from the secretory site and taken back to the vesicles, either unchanged or metabolized by monoamine oxidase (MAO). If it reaches the circulation, NE, and also EPI, are metabolized by MAO and catechol‐O‐methyltransferase (CMT) in the liver and kidney.
D Receptors on the effector organs
Cholinergic receptors are subdivided into muscarinic and nicotinic.
Muscarinic receptors are present in all effector cells stimulated by the postganglionic PNS neurons, as well as in those stimulated by the postganglionic SNS cholinergic neurons. Subtypes of muscarinic receptors are described in Table 7.1.
Nicotinic receptors are found in the synapses between the preganglionic and postganglionic neurons of the SNS and PNS, and at the neuromuscular junction.
ACh is the neurotransmitter at all cholinergic receptors.
Adrenergic receptors are subdivided into alpha (α1 and α2), beta (β1 and β2), and dopaminergic (DA).
Norepinephrine (NE) excites α receptors more than β receptors.
Epinephrine (EPI) excites α and β receptors approximately equally.
Dopaminergic receptors
There are five subtypes of dopaminergic receptors, D1 to D5. Dopaminergic receptors are primarily present in the CNS but are also present in the periphery.
Dopamine can act by three mechanisms:It modulates the release of norepinephrine from adrenergic neurons.It activates α and β receptors.It activates dopaminergic receptors.
Table 7.1 Muscarinic receptor subtypes.
| M1 | M2 | M3 | M4 | M5 | |
|---|---|---|---|---|---|
| Location | CNSStomach | HeartCNS | CNSSalivary glands; airway smooth muscle | CNSHeart? | CNS |
| Clinical effects | H+ secretion | Bradycardia | Salivation | ? | ? |
III Function of the adrenal medulla
A SNS innervation of the adrenals
Stimulation of the SNS nerves to the adrenal medulla causes large quantities of EPI and NE to be released into the bloodstream.
Approximately 80% of the secretion is EPI and 20% is NE.
B Effect of NE release from adrenals
The circulating NE causes constriction of most blood vessels, increased activity of the heart, inhibition of the GI tract, and dilation of the pupils.
C Effect of EPI release from adrenals
EPI, because it has greater affinity for β receptors, has a more profound effect on cardiac stimulation than does NE. However, NE is a more potent vasoconstrictor.
NE and EPI increase systemic vascular resistance, mean arterial pressure and cardiac output through their α‐ and β‐receptor activity. Heart rate is more likely to increase with EPI due to a stronger chronotropic effect, whereas it decreases with NE, as a result of a baroreflex in response to the increase in systemic vascular resistance.
IV
