ANS- 2A Flashcards
motor (efferent) nervous system
-2 components:
-somatic and autonomic
-distinguished by the types of effector organs they innervate and the types of functions they control
somatic nervous system
-voluntary motor system
-conscious
-pathways consist of single motoneuron and skeletal muscle fibers it innervates
-cell body of motoneuron is located in CNS (brain or spinal cord)
-its axons synapse directly on skeletal muscles
-ACh released from presynaptic terminals of motoneurons -> activates nicotinic receptors on motor end plates of skeletal muscle
autonomic nervous system
-2 divisions: sympathetic + parasympathetic
-involuntary
-controls and modulates functions on visceral organs
-pathways have preganglionic and postganglionic
-preganglionic cell body- CNS
-postganglionic cell body- autonomic ganglia located outside CNS
-preganglion release ACh
-postganglion release ACh or norepinephrine or in some cases neuropeptides
sympathetic preganglion
-originate in nuclei of thoracolumbar spinal cord
-leave the spinal cord via ventral motor roots and white rami
-project either to prevertebral ganglia of sympathetic chain or to series of prevertebral ganglia
-T1-L3
-sympathetic division = thoracolumbar
-always cholinergic -> release ACh
-interact with nicotinic (N2) receptors on cell bodies of postganglia
parasympathetic preganglion
-originate the brain stem and sacral spinal cord
Adrenergic neurons
-release norepinephrine or epinephrine
-receptors for norepinephrine on effector organs are called adrenoreceptors
-either sympathetic or parasympathetic
-norepinephrine or epinephrine is secreted into circulation by adrenal medulla
-postganglion can be adrenergic or cholinergic
cholinergic neurons
-release acetylcholine (ACh)
-receptors for ACh -> cholinoreceptors
-either sympathetic or parasympathetic, ALL preganglionic neurons release ACh
-postganglion can be adrenergic or cholinergic
neuroeffector junctions
-junctions between postganglionic autonomic neurons and their effectors
-analogous to neuromuscular junctions of the somatic nervous system*
-postganglionic neurons innervate target tissues form DIFFUSE branching networks
-beads, or varicosities* line these branches and are sites of neurotransmitter synthesis, storage, and release
-varicosities are analogous to presynaptic nerve terminals of NMJ
-overlap in branching networks from different postganglionic neurons -> target tissues may be innervated by many postganglionic neurons
-postsynaptic receptors are widely distributed on target tissues
-there is no specialized region of receptors analogous to motor end plate of skeletal muscle
neuromuscular junction
-somatic nervous system
-effector (skeletal muscle fiber) is innervated by single motoneuron
sympathetic nervous system
-mobilize body for activity
-fight or flight
-increased arterial pressure, increased blood flow to active muscles, increased metabolic rate, increased blood glucose concentration, increased mental activity and alertness
paravertebral ganglia
-preganglionic neuron synapses on postganglionic neurons in paravertebral ganglia of sympathetic chain
-occur in ganglia at same segmental level of chain OR preganglion may turn in the cranial or caudal direction and innervate ganglia at higher or lower levels in the chain -> allow for synapse in multiple ganglia
prevertebral ganglia
-preganglion can pass through sympathetic chain without synapsing and continues on to synapse in prevertebral ganglia
-celiac, superior mesenteric, inferior mesenteric
-supply visceral organs, glands, and enteric nervous system of GI tract
-postganglion travel to periphery and innervate effector organs
sympathetic pathways
-preganglia originating in upper thoracic spinal cord-> thorax (heart)
-preganglia originating in lumbar spinal cord -> pelvic (colon, genitals)
-blood vessels, thermoregulatory sweat glands, pilomotor muscles of skin -> preganglionic neurons synapse on multiple postganglionic neurons up and down sympathetic chain -> broad distribution throughout body
-superior cervical ganglion -> head (eyes, salivary glands)
-celiac ganglion -> stomach and small intestine
-superior mesenteric ganglion -> small and large intestine
-inferior mesenteric ganglion -> lower large intestine, anus, bladder, and genitalia
adrenal medulla
-specialized sympathetic ganglion
-ANS
-preganglionic neurons originate thoracic spinal cord (T5-T9) -> pass through sympathetic chain and celiac ganglion without synapsing -> travel in greater splanchnic nerve to adrenal medulla
-synapse on chromaffin cells -> release ACh -> activates nicotinic receptors
-when activated chromaffin cells secrete catecholamines (epinephrine and norepinephrine) into circulation-> AS A HORMONE bc its systemic
sympathetic postganglionic neurons
-adrenergic in all effector organs EXCEPT thermoregulatory sweat glands (cholinergic)
-when stimulated -> norepinephrine and ATP are leased from small dense core vesicles
-these neurotransmitters at the neuroeffector junction -> bind to and activate their respective receptors on target tissue (vascular smooth muscle)
thermoregulatory sweat glands
-only sympathetic postganglia that are cholinergic (the rest are adrenergic)
-innervated by sympathetic cholinergic neurons have muscarinic cholinoreceptors
parasympathetic nervous system
-restorative, conserve energy
-preganglia cell bodies in either brain stem (midbrain, pons, medulla) or sacral spinal cord
-preganglia axons project to series of ganglia located near effector organs
-ganglia located near, on, or in effector organs
parasympathetic preganglionic neurons
-arise from nuclei of cranial nerves (3,7,9,10) or sacral spinal cord (S2-S4) -> craniosacral
-ganglia located near, on, or in effector organs
-long axons
-cholinergic and release ACh -> interacts with nicotinic (N2) receptors on cell bodies
parasympathetic postganglionic neurons
-parasympathetic postganglionic neurons are typically cholinergic as well
-when stimulated ACh is released from varicosities and bind to muscarinic receptors on target tissue
-high frequency stimulation (intense)- large dense core vesicles release their peptides -> bind to receptors on target tissue and augment the actions of ACh
micturition
-voluntary but sensation is autonomic
-emptying bladder is voluntary bc external sphincter is skeletal
-micturition reflex -> ANS
-detrusor muscle of bladder wall (body) and internal bladder sphincter are composed of smooth muscle -> innervated sympathetic and parasympathetically
-reflex occurs when bladder senses being full
-sympathetic -> bladder filling
-detrusor relaxed filling- beta 2
-sphincter contracted filling- alpha 1
-parasympathetic-> bladder emptying
-detrusor is contracted- M
-sphincter relaxed- M
-relaxed and contracted emptying- muscarinic
size of pupil
-controlled by 2 muscles of iris: pupillary dilator (radial) and pupillary constrictors (sphincter)
-pupillary dilator muscle- sympathetic innervation through alpha 1 receptors -> constrict radial muscle -> dilation (mydriasis)
-pupillary constrictor muscle- parasympathetic innervation through muscarinic receptors -> constriction sphincter muscle -> constriction of pupil (miosis)
pupillary light reflex
-light strikes retina and activates parasympathetic preganglionic nerves in Edinger-Westphal nucleus
-activation of parasympathetic fibers cause contraction of sphincter muscle and pupillary constriction
-accommodation response- blurred retinal image activates parasympathetic preganglionic neurons in Edinger-Westphal nuclei -> leads to contraction of sphincter muscle and pupillary constriction
-at same time, ciliary muscle contracts causing the lens to round up and its refractive power to increase
gastrointestinal tract
-contraction of wall of GI tract is accompanied by relaxation of sphincters (parasympathetic)
-allows the contents to propel forward
-relaxation of wall of GI is accompanied by contraction of sphincters (sympathetic)
-combined effect of these is to slow or stop movement of contents
sympathetic and parasympathetic innervation generalization
-parasympathetic- effector organs have muscarinic receptors
-sympathetic- multiple receptor types in effector organs -> 4 adrenoreceptors (alpha1, alpha2, beta1, beta2) + muscarinic receptors
-sympathetic adrenoreceptor- receptor type is related to function
alpha 1 receptors
-cause contraction of smooth muscles
-vascular smooth muscle, GI and bladder sphincters, pilomotor muscles, radial muscles of iris
-epinephrine is slightly more potent
-relatively insensitive to catecholamines
-requires a lot of catecholamines for activation -> this happens locally from postganglionic sympathetic adrenergic nerve fibers (norepinephrine)
-not epinephrine from medulla
beta 1 receptors
-involved in metabolic functions
-gluconeogenesis, lipolysis, renin secretion, all functions in the heart
-epinephrine and norepinephrine equipotent at beta 1
beta 2 receptors
-cause relaxation of smooth muscle in bronchioles, wall of bladder, and wall of GI
-preferentially activated by epinephrine from adrenal medulla
A 48-year-old woman visits her PA complaining of what she calls “panic attacks.” She reports that she has experienced a racing heart and that
she can feel (and even see) her heart pounding in her chest. She also complains of throbbing headaches, cold
hands and cold feet, feeling hot, visual
disturbances, and nausea and vomiting. In the PAs office, her blood pressure is severely elevated (230/125). She is admitted to the hospital for evaluation of her hypertension. A 24-hour urine sample reveals elevated levels of
metanephrine, normetanephrine, and 3-methoxy-4-hydroxymandelic acid (VMA). After the physician rules out other causes for hypertension, he concludes that she has a tumor of the adrenal medulla, called a pheochromocytoma. A computerized tomographic scan of the abdomen reveals a 3.5-cm mass on her right adrenal medulla. The patient is administered an α1 antagonist,
and surgery is performed. The woman recovers fully; her blood pressure returns to normal, and her other symptoms disappear.
-pheochromocytoma, a tumor of the chromaffin cells of the adrenal medulla
-tumor secretes excessive
norepinephrine and epinephrine -> elevated catecholamine metabolites in her urine
-normally adrenal medulla secretes mainly epinephrine, but pheochromocytomas secrete mainly norepinephrine
-tissue with adrenoreceptors (heart and blood vessels) -> activated by elevated epinephrine and norepinephrine
-β1 receptors in the heart are activated -> increase heart rate and contractility
-Activation of α1 receptors in vascular smooth muscle of the skin -> vasoconstriction-> cold hands and feet
-vasoconstriction also impairs ability to dissipate heat-> she is hot
-elevated BP->increased heart rate, increased contractility, and
increased constriction (resistance) of the blood vessels.
-headache secondary to BP
-activation of adrenoreceptors in other organ systems (i.e., gastrointestinal symptoms of nausea and vomiting and visual disturbances).
pheochromocytoma treatment
-locating and excising the tumor
-removing source of excess catecholamines
-woman could have been treated pharmacologically with combo of
α1 antagonists (e.g., phenoxybenzamine or prazosin) and β1 antagonists (e.g., propranolol)
-prevents actions of the endogenous catecholamines at the receptor level.
A 66-year-old man who suffered a stroke on the right side has a drooping right eyelid (ptosis), constriction of his right pupil (miosis), and lack of sweating on the right side of his face (anhidrosis). His physician orders a test with cocaine
eye drops. When a solution of 10% cocaine is applied in the left eye, it causes dilation of the pupil (mydriasis). However, when the cocaine solution is applied in the right eye, it fails to cause dilation of that pupil.
-Horner syndrome, secondary to his stroke
-loss of sympathetic innervation to smooth muscle elevating the right eyelid -> ptosis on the right side
-loss of sympathetic innervation on the right pupillary dilator -> constriction of right pupil
-loss of sympathetic innervation of right sweat glands on face > anhidrosis on the right
-cocaine drops were instilled in the left eye (unaffected side), the cocaine blocked reuptake of norepinephrine into sympathetic nerves innervating the
pupillary dilator muscle -> less norepinephrine -> no pupillary dilation
-higher norepinephrine levels in those adrenergic synapses -> constriction of radial muscle of the iris -> prolonged dilation of the pupil
-treatment is to address underling cause
A 58-year old man in seemingly good health begins to experience alarming symptoms. He is occasionally impotent, and recently his impotence has progressed to “every time.” In addition, he has enormous urgency to urinate but has difficulty producing a urinary stream. He has been reluctant to seek medical attention for these issues, but
one morning, he faints when he arises from bed. By the time he schedules an appointment with his physician, he is dizzy every morning and has a wide array of symptoms, including double vision, indigestion, diarrhea, and heat intolerance. The man is referred to a neurologist, who performs an ocular test that involves instilling methacholine into
the conjunctival sac; in this man, the methacholine causes exaggerated miosis (constriction of the pupil due to contraction of circular muscle of the iris).
Because of the global nature of the man’s symptoms and the results of this ocular test, the neurologist diagnoses him with Shy-Drager syndrome.
-shy-drager syndrome is rare progressive disease of central ANS associated with degeneration of preganglionic neurons of intermediolateral cell column of spinal cored, peripheral autonomic ganglia, and hypothalamic autonomic centers
-severe impairment in both sympathetic and parasympathetic
-impotence, difficulty urinating, heat intolerance-> para and sympathetic dysfunction
-erection - parasympathetic, muscarinic receptors
-ejaculation- sympathetic alpha 1 receptors
-destrusor muscle of bladder wall is composed of smooth muscle with sympathetic (beta 2) and parasympathetic (muscarinic) innervation
-internal bladder sphincter is composed of smooth muscle with sympathetic (alpha 1) and parasympathetic (muscarinic) innervation
-thermoregulatory - sympathetic
-exaggerated ocular response to methacholine (cholinergic muscarinic agonist) -> perhaps surprising, since the man’s parasympathetic nervous system is
impaired; however, the test results make sense because the loss of parasympathetic innervation to circular muscle of the iris causes up-regulation of cholinergic receptors and thus an enhanced response to an exogenously applied cholinergic agonist (denervation
hypersensitivity)
-orthostatic hypotension (decrease in BP upon standing up) -> blood pools in lower extremities -> decreases arterial pressure
-because his baroreceptor (controlled by para and sympathetic) is impaired -> dizzy and fainted
shy-drager syndrome treatment
-elevated head during sleep
-lessen orthostatic effects on BP upon standing
-wear compression stockings to prevent blood from pooling in legs
-take aldosterone analogue to increase blood volume
-attempts to ameliorate dizziness and fainting upon standing up
-treatment is palliative
-no cure
-fatal degenerative disease
CASE. A woman planning a
10-day cruise asks her physician for medication to
prevent motion sickness. The physician prescribes scopolamine, a drug related to atropine, and recommends that she take it for the entire duration of the cruise. While taking the drug, the woman experiences no nausea or vomiting, as hoped. However, she does experience dry mouth, dilation of the pupils (mydriasis), increased heart rate (tachycardia), and difficulty voiding urine.
-scopolamine (like atropine) block cholinergic muscarinic receptors in target tissue
-used effectively to treat motion sickness
-adverse effect
-activation of muscarinic receptors causes increased salivation, constriction of pupils, decreased heart rate (bradycardia) and contraction of bladder wall during voiding
-inhibition of muscarinic receptors with scopolamine -> decreased salivation (dry mouth), dilation of pupils (unopposed influences of sympathetic on radial muscles), increased HR, slowed voiding of urine (caused by loss of contractile tone of bladder wall)
-treatment- discontinue scopolamine
sympathetic response: target organs
-pupil dilation
-suppression of submandibular, sublingual, parotid glands- dry mouth
-heart rate increase- oxygen supplies muscle
-increase contractility- SV + CO increase
-bronchodilation
-decrease digestion- blood shunts away from stomach, small and large intestine -> blood prioritizes muscle perfusion
-adrenal medulla stimulated- norepinephrine and epinephrine released -> systemic response
-urinary bladder relaxes (allows for movement of fluid) and contraction of sphincter
-male genitalia- ejaculation
parasympathetic response: target organs
-pupil constriction
-lacrimal, nasal, parotid, submandibular, sublingual gland stimulation- digest
-decrease heart rate- vagus nerve innervates SA node to lower base line rate
-bronchoconstriction
-stomach, small and large intestine- increase blood, secretion -> digest, nutrient absorption
-urinary bladder- sphincter relaxed and bladder constricted
-male genitalia- erection
norepinephrine
-smooth muscle
-alpha receptors -> contract
-beta receptors -> dilate
-sympathetic stimulation releases norepinephrine and dilates and contracts target organ depending on the receptors they have
baseline
-sympathetic is usually always more prevalent than parasympathetic
-parasympathetic brings us to baseline
autonomic regulation
-hypothalamus and brain stem
-temperature regulation, thirst, food intake, micturition, breathing, and cardiovascular (vasomotor) function
-vasomotor center- receives information about BP from baroreceptors in carotid sinus and compares to blood pressure set point
-influence sympathetic and parasympathetic innervation to heart and blood vessels
autonomic receptors
-at NMJ, cell bodies of postganglionic neurons, effector organs
-beta 1 in SA node is coupled to mechanisms that increase spontaneous rate of depolarization and increase HR
-binding of norepinephrine to B1 in SA node increases HR
-B1 in ventricular muscle is coupled to mechanisms that increase Ca2+ concentration and contractility
-binding of norepinephrine in B1 in ventricles increases contractility but no direct effect on heart rate
G proteins
-autonomic receptors are coupled to GTP binding proteins
-G protein linked receptors
-composed of single polypeptide chain that winds back and forth across the cell membrane 7 times -> 7 pass transmembrane receptor proteins
-ligand (ACh, norepinephrine) binds to extracellular domain of G protein liked receptor
-intracellular domain of receptor binds G protein
-G protein couple G protein linked autonomic receptors to enzymes that execute physiologic actions
norepinephrine
-released from postganglionic sympathetic adrenergic nerve fibers
epinephrine
-released from adrenal medulla
nicotinic receptors
-motor end plate, ALL autonomic ganglia (para and symp), on chromaffin cell of adrenal medulla
muscarinic receptors
-all effector organs of parasympathetic division and few effector organs of sympathetic division
-heart, GI, bronchioles, bladder, male sex organs
cholinergic drugs
-salivation, lacrimation, defecation, urination
-cholinergic agonist enhance parasympathetic tone
parasympathetic stimulation
-decrease HR, conduction, contractility
-release EDRF
-constricts bronchioles and circular sphincter (constricts pupils -> miosis)
-contracts smooth muscle GI, detrusor muscle, ciliary muscle (near vision)
-secretion lacrimal glands
-relaxes GI and bladder sphincter
-increase saliva secretion, gastric acid, and pancreatic secretion
-erection
