Chapter 2 Peripheral nervous system drugs - general information

Question 1

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Fight or flight response (sympathetic nervous system)

Answer 1

• provides energy, catabolic
• less lung secretions, bronchodilation (inc blood oxygenation)
• increased heart rate and contractility
• arteriolar constriction shunts blood from skin and digestive tract WHILE arterioles in heart and skeletal muscle dilate to supply more blood to those organs
• Glycogen and lipids breakdown => glucose for ENERGY
• GI motility and secretions decrease
• Urine retained (can’t fight a bear when you are pooping or peeing hehe)
• dilated pupils

Question 2

Parasympathetic pig’s heart

Answer 2

• slow HR
• increased secretions (saliva in mouth and mucus in nose) – help with digestion and breathing during times of rest
• inc’d bowel movement
• bronchioles constricted (less work for lungs)
• constricted pupils (limits light to your eyes)
• relaxes muscles to help you pee + poop
• enhance reproductive organs (fluids + erection)
• increased digestion (insulin release) + urination

Question 3

ganglionic transmission

Answer 3

1) presynaptic neurons (preganglionic neurons – originate in brain stem or spinal cord)
* release acetylcholine
2) presynaptic neurons stimulate nicotinic ganglionic receptors on post-ganglionic neurons (autonomic system) [postsynaptic neurons]
* sympathetic ganglia ==> located along spinal cord (release norepinephrine usually)
* parasympathetic ganglia ==> lie near end organs (release acetylcholine)

EXCEPTION ===================
acetylcholine activates sweat glands (sympathetic nervous)
* NEUROMUSCULAR transmission
1) neurons release acetylcholine (from brain and stem => skeletal muscles); no intermediate receptors; directly controls muscles
2) these released acetylcholine bind to nicotinic muscle receptors on muscle cells => causing calcium influx

• central neurotransmission - acetylcholien is a NT in the brain, activating via muscarinic receptors

Question 4

Norepinephrine synthesis, release, and degradation

Answer 4

• amino acid Tyrosine => dopa (hydroxylated) => dopamine (decarboxylated) ni presynpatic neuron
• Dopamine goes into enzyme (dopamine B-hydroxylase) => form norepinephrine
• # when this nerve portion is stimulated, Ca++ enters presynaptic neuron and relesaed norepinephrine into cleft using storage vesicle
• now acetylcholine may bind to => a1 adrenergic, b1 adrenergic or b2 adrenergic receptor (direct sympathomimetic drugs or adrenergic drugs — thye can bind to those same target receptors w/o interacting with the presynaptic neuron)
• FOR a2 presynaptic receptors – stimulation of them w/ by norepinephrine (located on presynaptic neurons as well) inhibits subsequnt release of norepinephrine from presynpatic terminal

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Degrading and recycling of norepinephrine
1) enzyme catechol-o-methyl (sounds like catecholamine) transferese breaks down norepinephrine (including epinephrine, dopamine)
2) commonly – excess norepinephrine transported back into presynaptic neuron (then it is repacked in storage vesicles or degraded by mitochondrial monoamine oxidase)
NOTE – indirect sympathomimetics — drugs that work by entering presynaptic terminal and displacing norepinephrine (versus direct)

Question 5

Acetylcholine synthesis, release, and degradation

Answer 5

1) choline + acetyl CoA (enzyme choline acetyltransferase catalyzes them) => acetylcholine
2) stored in storage vesicles then released after action potential
3) may bind to Nm receptors (nicotinic receptors on muscles cells)
4) OR Ng receptors (nicotinic receptors on ganglionic synapses of autonomic nervous system) – postsynaptic neurons
5) or M1, M2, M3 muscarinic receptors

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6) @ synaptic cleft, acetylcholine is removed via hydrolysis (into choline) — which is actively reabsorbed back into presynaptic terminal
7) additionally, acetycholine breakdown producted are recycled back into acetylcholine