Flashcards in Test 2 Lectures 2-4 Deck (80)
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1
Which is the craniosacral vs. thoracolumbar division of the spinal cord? Which has longer post- or pre-ganglionic neurons?
1. Sympathetic - thoracolumbar division (short pre-ganglionic cells and long-post
ganglionic cells)
2. Parasympathetic - craniosacral division (long pre-ganglionic cells and short
post-ganglionic cells)
2
A .Pre-ganglionic fibers release __________.
B. Post-ganglionic parasympathetic fibers release _________.
C. Post-ganglionic sympathetic fibers release _________.
D. Adrenal medulla releases _________and ________ (to a lesser extent) into
the circulation
E. Exceptions: Post-ganglionic sympathetic fibers that innervate sweat glands
and some skeletal muscle blood vessels that release _________.
- ACh
- ACh
- NE
- Epi, NE
- ACh
3
Is accommodation regulated by symp or parasymp?
Parasymp
4
Describe the 4 autonomic influences on the eye (symp vs. parasymp and their function)
Dilator: constrict it to open the pupil (symp)
- Could prevent aqueous humor from draining effectively or to visualize eye
Sphincter contraction would release pressure (parasymp)
- Parasymp agonists help flatten iris--aqueous humor drainage
Ciliary mm. (parasymp)
- Helps change of lens to promote accommodation
- Also helps w/promoting drainage!
Ciliary epithelium (symp)
- Makes aqueous humor
5
How does sympathetic activation affect HR? (what currents are affected and how?) (what phase # does this take place during?)
Sympathetic activation increases inward calcium current and the funny current to promote faster spontaneous depolarization during phase 4 of sinoatrial node action potential and lower threshold for activation
6
How does sympathetic activation affect heart contractility?
Sympathetic activation also stimulates greater calcium influx into myocytes during depolarization culminating in greater contractile force of the heart.
7
What enzyme converts dopamine to NE in vesicles?
Dopamine beta-hydroxylase
8
What are the 3 routes of termination of an action potential in a sympathetic neuron?
1) re-uptake into nerve terminals or post-synaptic cell
2) diffusion out of synaptic cleft
3) metabolic transformation
9
Where are alpha-1 receptors expressed?
What are the effects?
1. Most vascular smooth muscle
2. Pupillary dilator muscle
1. Contracts (^ vascular resistance)
2. Contracts (mydriasis)
10
Where are alpha-2 receptors expressed?
What are the effects?
1. Adrenergic and cholinergic nerve terminals (pre-synaptically)
2. Some vascular smooth muscle (like alpha-1)
1. Inhibits NT release
2. Contracts (^ vascular resistance)
11
Where are beta-1 receptors expressed?
What are the effects?
1. Heart
2. Juxtaglomerular cells
1. Stimulates rate and force
2. Stimulates renin release
12
Where are beta-2 receptors expressed?
What are the effects?
1. Respiratory, uterine, and vascular smooth muscles
2. Somatic motor nerve terminals (voluntary muscle)
1. Relaxation (unlike alpha-1/2)
2. Causes tremor
13
Where are dopamine-1 receptors expressed?
What are the effects?
1. Renal and other splanchnic blood vessels
1. Relaxes (reduces resistance)
14
Eye – activation of dilator muscle causes ___________ (mydriasis vs miosis), innervation of ciliary epithelium
regulates production of ____________.
- mydriasis
- Aqueous humor
15
Constricting pupillary dilator muscle __________ drainage, while relaxation __________ drainage.
- Prevents
- Promotes
16
Describe the pharmacological mechanism of action of alpha-1 adrenergic receptors produces smooth m. contraction.
Binding -> Gq -> PLC -> PIP2 -> DAG + (soluble) IP3 -> Ca2+ release -> smooth m. contraction
17
Describe the pharmacological mechanism of action of alpha-2 adrenergic receptors reduce presynaptic NT release.
Binding -> Gi -> inhibits AC/cAMP/PKA -> reduced P'lation of presynaptic N-type Ca2+ channel -> reduced Ca2+ release -> reduced NT release (presynaptically)
18
Describe the pharmacological mechanism of action of beta-1 adrenergic receptors produce their effects on the heart.
Binding -> Gs -> AC/cAMP/PKA -> increased Na+ (funny current) and P'lation of L-type Ca2+ channels -> increased sarcoplasmic Ca2+ storage + release -> chronotropy (SA node cells) and inotropy (cardiomyocytes)
19
Describe the pharmacological mechanism of action of beta-2 adrenergic receptors reduce smooth m. contraction in the uterus, bronchioles, and vascular smooth m.
Binding -> Gs -> AC/cAMP/PKA -> P'lates (and inhibits) MLCK -> reduced affinity for Ca/calmodulin -> decreased P'lation of myosin -> reduced smooth m. contraction.
20
Describe the pharmacological mechanism of action of alpha-2 adrenergic receptors produce peripheral vasoconstriction.
Binding -> Gi -> inhibits AC/cAMP/PKA -> decreased P'lation of MLCK -> increased affinity for Ca/calmodulin -> P'lation of myosin -> smooth m. contraction
21
What are the 3 endogenous ligands for adrenergic receptors?
NE, EPI and dopamine (DA)
22
Recall: what degrades each of the catecholamines (NE, epi, DA) after their release?
COMT: Epi, NE, DA
MAO: NE, DA
23
Give the relative affinity for the alpha1 adrenergic receptor of NE, EPI, and isoproterenol
Epi ≥ NE >> isoproterenol (negligible binding)
24
Give the relative affinity for the alpha2 adrenergic receptor of NE, EPI, and isoproterenol
Epi ≥ NE >> isoproterenol (negligible binding)
25
Give the relative affinity for the beta1 adrenergic receptor of NE, EPI, and isoproterenol
Isoproterenol > epi >> NE
(NE lacks ability to relax smooth m.)
26
Give the relative affinity for the beta2 adrenergic receptor of NE, EPI, and isoproterenol
Isoproterenol > epi = NE
27
MAP =
CO x TPR
28
CO =
HR x SV
29
TPR has a predominant effect on __________ (systolic/diastolic) pressure, while CO has a predominant effect on ___________ (systolic/diastolic) pressure.
- diastolic
- systolic
30
