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Pharm > Autonomic Intro > Flashcards

Autonomic Intro Flashcards

1
Q
  1. What are the classifications of the nervous system?
A

Nervous system → somatic nervous system, autonomic nervous system
Autonomic nervous system → parasympathetic (craniosacral) and sympathetic (thoracolumnar) nervous system
*Parasympathetic is dominant over sympathetic!

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2
Q
  1. What is the exception to the two-neuron arrangement of the ANS?
A

Innervation of the adrenal medulla which secrets catecholamines (NE, E) in replace of a 2nd neuron

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3
Q
  1. When is the sympathetic system stimulated?
A

Trauma, fear, hypoglycemia, cold, exercise

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4
Q
  1. What are general effects of the sympathetic nervous system?
A
  1. increase HR and blood pressure
  2. mobilization of energy stores
  3. increase in blood flow to skeletal muscles in the heart
  4. dilation of pupils
  5. dilation of bronchioles
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5
Q
  1. What is the main control of the heart and blood pressure?
A

Heart → parasympathetic

Blood pressure → sympathetic

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6
Q
  1. Which fibers synthesize and release Ach?
A
  1. all preganglionic efferent autonomic fibers
  2. all parasympathetic postganglionic fibers
  3. all somatic motor fibers to skeletal muscle
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7
Q
  1. Which fibers synthesize and release norepinephrine?
A

Postganglionic sympathetic fibers

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8
Q
  1. What are the exceptions to postganglionic sympathetic fibers that release norepinephrine?
A
  1. sympathetics that supply the sweat glands → release Ach
  2. Adrenal medulla releases NE and E
  3. Dopamine is released by some sympathetic fibers (renal vascular smooth muscle??)
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9
Q
  1. Discuss the Acetylcholine is produced and broken down.
A
  1. Choline is transported from extracellular fluid into neurons via sodium-dependent carrier (CHT1) [**rate limiting step of Ach production]
  2. Acetyl-CoA is synthesized in mitochondria
  3. acetyl-CoA + choline → Acetylcholine via choline acetyltransferase [in cytoplasm]
  4. Ach is transported from cytoplasm into vesicle via vesicular ACh transporter (VAChT) which is an antiporter that coupled ACh influx with H+ efflux
  5. Release of these vesicles into postsynaptic cleft relies on extracellular calcium to be sufficient enough to trigger an AP
  6. Release Ach binds to and activates Ach receptors on post-synaptic cell
  7. Acetylcholinesterase (AChE) splits acetylcholine into choline and acetate terminating action of transmitter
  8. Butyrylcholinesterase is a cholinesterase with lower specificity compared to AChE that is found in blood plasma, liver and other tissues
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10
Q
  1. Discuss the production and release of NE and E.
A
  1. tyrosine amino acid is transported across BBB via system L which is Na+ independent
  2. Once tyrosine enters neuron [*rate limiting step] it is converted to L-DOPA via tyrosine hydroxylase
  3. DOPA is then converted to dopamine by aromatic L-amino acid decarboxylase (DOPA decarboxylase)
  4. Vesicular monoamine transporter (VMAT) translocates dopamine into synaptic vesicle in exchange for H+
  5. In the vesicle, dopamine is converted to norepinephrine via dopamine-B-hydroxylase
  6. *in the adrenal medulla, NE moves to the cytosol where phenylethanolamine N-methyltransferase (PNMT) converts norepinephrine to epinephrine
  7. Release of vesicles are calcium dependent
  8. Once released NE and E are metabolized by catechol-O-methyltransferase and MAO
  9. Termination also occurs from simple diffusion away from receptor site and back to nerve terminal
  10. Termination can also occur from reuptake of NE via NET (Na+ dependent norepinephrine transporter) aka uptake 1
  11. **note that indirectly-acting sympathomimetics (tyramine and amphetamines) can also be taken up into noradrenergic nerve endings via uptake 1 displacing NE from storage vesicles
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11
Q
  1. What is COMT?
A

Catechol-O-methyltransferase and monoamino oxidase → soluble or RER-membrane bound – it catalyzes transfer of methyl group to –OH of catechol

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12
Q
  1. What is MAO?
A

Enzyme located in outer membrane of mitochondria in most neurons. MOA oxidatively deaminates monoamines to aldehydes then to glycols. There exists MAO-A and MAO-B. MAO-A deaminates NE, E, and serotonin. MAO-B deaminates dopamine.

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13
Q
  1. What are the different cholinergic receptors?
A
  1. muscarinic → G protein-linked

2. nicotinic → ion channel-linked [2 Ach molecules bind opening channel and allowing Na+ influx]

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14
Q
  1. What are the different types of nicotinic receptors?
A
  1. muscle type (Nm) – skeletal neuromuscular junction (NMJ)

2. neuronal type (Nn) – found in autonomic ganglia and brain

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15
Q
  1. Where are muscarinic receptors located?
A
  1. plasma membrane of cells in the CNS
  2. organs innervated by parasympathetic nerves
  3. tissues innervated by cholinergic postganglionic sympathetic nerves
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16
Q
  1. What are the different types of muscarinic receptors?
A
  1. M1 – Gq, found on ganglia, causes depolarization
  2. M2 – Gi, causes cardiac inhibition in heart, causes release of transmitters from presynaptic nerve terminals
  3. M3 – Gq, smooth muscle contraction, secretory gland secretion, vascular endothelium vasodilation (via NO)
17
Q
  1. How do M3 receptors mediation relaxation of vascular smooth muscle?
A

M3 receptors are present on endothelial cells of the vasculature. These cells also contain NO synthase (eNOS). eNOS catalyzes the formation of NO from arginine. Activation of M3 receptors causes increase in intracellular calcium mediated by Gq. The calcium activates eNOS leading to formation of NO from arginine. The NO then diffuses from the endothelial cells into the adjacent smooth muscle cells. NO in the smooth muscle cells binds and activates guanylyl cyclase producing cGMP from GTP. cGMP activates cGMP-dependent protein kinase which phosphorylates proteins leading to relaxation fo the SM wall resulting in vasodilation.

18
Q
  1. What are the different types of adrenergic receptors?
A
  1. a-adrenoceptors
  2. B-adrenoceptors
    * *All are G protein linked
19
Q
  1. What neurotransmitters activate what B-adrenergic receptors?
A

B1 and B3 have approximately equal affinity for epinephrine and norepinephrine. B2 has higher affinity for epinephrine than norepinephrine. ALL B adrenergic receptors stimulate adenylyl cyclase via interaction with Gs.

20
Q
  1. What is the effect of B1 adrenergic receptors?
A

Gs (increase cAMP and Ca2+), acting on the heart to increase heart rate, force and AV conduction velocity and on the juxtaglomerular cells to increase renin release

21
Q
  1. What is the effect of B2 adrenergic receptors?
A

Gs (increase cAMP)

  1. smooth muscle relaxation
  2. skeletal muscle → increase glycogenolysis, increase K+ uptake
  3. Pancreatic B cells → increase insulin secretion
  4. Pancreatic a cells → increase glucagon secretion
  5. Liver → increase glycogenolysis and gluconeogenesis
22
Q
  1. What is the effect of B3 adrenergic receptors?
A

Gs (increase cAMP) → increase lipolysis in adipocytes

23
Q
  1. What are the different a-adrenergic receptors?
A
  1. a1 → Gq pathway

2. a2 → Gi pathway (decreases Ca2+) and increases Ca2+

24
Q
  1. What is the effect of the a1 adrenergic receptors?
A

Gq (increased IP3, DAG, Ca2+)

  1. vascular smooth muscle contraction
  2. genitourinary smooth muscle contraction
  3. liver → increased glycogenolysis and gluconeogenesis
25
Q
  1. What is the effect of the a2 adrenergic receptors?
A

Gi (decreased cAMP, decreased Ca2+, increased K+)
1. presynaptic nerve terminals → inhibition of NE and ACh release
2. platelets → aggregation
3. adipocytes → inhibition of lipolysis
4. pancreatic B cells → decreased insulin secretion
AND increased Ca2+ → contraction of vascular smooth muscle

26
Q
  1. What are the different dopaminergic receptors?
A

D1, D5 → Gs (increase cAMP) causing relaxation of the smooth muscle of the renal vascular bed

27
Q
  1. What is the primary controlled variable in the cardiovascular system?
A

Mean arterial pressure

*changes that alter the MAP evokes homeostatic secondary responses that directly compensate for the change

28
Q
  1. Give an example of norepinephrine infusion and a homeostatic compensatory change.
A

NE produces a direct effect on both vascular and cardiac muscle leading to vasoconstriction of peripheral vasculature causing an increase in MAP. Without a reflex, NE would increase HR and contractive force via a B1 effect. BUT people with reflexes have negative feedback baroreceptors that respond to increased MAP causing decreased sympathetic outflow, resetting the heart and slowing the heart rate → bradycardia.

29
Q
  1. Which parts of the eye are controlled by the ANS, through what receptor and for what function?
A
  1. pupillary dilator muscle in iris (radial), a1 receptor, contracts causing mydriasis (pupil dilation)
  2. pupillary constrictor muscle in iris (sphincter), M3 receptor, contraction causes miosis
  3. ciliary muscle, M3 receptors, contraction adapts to short range focus and relaxation adapts to long range focus (accommodation)
  4. ciliary epithelium, B2 receptors, produces aqueous humor
30
Q
  1. What is the basic role of pilocarpine?
A

Muscarinic agonist that causes ciliary muscle contractions facilitating outflow of aqueous humor into canal of schlem reducing intraocular pressure – used to treat glaucoma

31
Q
  1. What is the basic role of Tropicamide?
A

Muscarinic antagonist that causes relaxation of pupillary constrictor muscle (sphincter) causing mydriasis (dilation) and relaxation of ciliary muscles allowing for accommodation of long distance vision focus (cycloplegia).

Pharm (28 decks)

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