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CV Week 3 > Autonomic Nervous System III > Flashcards

Autonomic Nervous System III Flashcards

0
Q

Table 4 understand the location, cellular effects, agonists, antagonists of M1, 2, and 3.

A

pp. 78

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1
Q

What are the organ distribution of parasympathetic receptors?

A

M1: gastric parietal cells, CNS, ganglia
M2: cardiac, atria, conducting tissue
M3: S mm, exocrine glands, endothelial cell
M4: confined to certain region of CNS (still under investigation)
M5: under investigation

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2
Q

Draw Figure (Table) 19 twice and understand the relationship.

A

pp. 79

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3
Q

Why is the name G-protein?

A

Because it requires GTP to function.

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4
Q

What is the G-protein utilized when Beta-adrenergic receptors are activated?

A

Gs- because it stimulates the cyclase.

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5
Q

What is the G-protein utilized when alpha 2-adrenergic receptors and M2 cholinergic receptors are activated?

A

Gi- because it inhibits the cyclase.

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6
Q

What is the G-protein utilized when alpha 1-adrenergic and M1 and M3 cholinergic receptors are activated?

A

Gq-activate phospholipase C (PLC)-hydrolyzes PIP2 into IP3 and DAG.

  • IP3 mobilize Ca from internal stores.
  • DAG activates PKC
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7
Q

How are the receptors in the ANS are related to the nervous system in general?

A

1) The same receptors found in the ANS are also present within the somatic and CNS.
2) Principles for the mode of action of receptors within the ANS also apply to CNS.

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8
Q

Discuss the effects mediated by adrenergic receptors.

A

TABLE 5 pp 81

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9
Q

What type of alpha-adrenergic receptors are found in S mm?

A

Alpha 1-adrenergic receptors are mainly found in S mm although there are alpha 2 in vascular S mm.

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10
Q

How do alpha 1 and alpha 2 work?

A

Alpha 1 via IP3 and DAG= increase in intracellular Ca (IP3) and activation of PKC (DAG)

Alpha 2 via inhibition of adenylyl cyclase and decrease of cAMP.

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11
Q

Use the example of vascular smooth mm to show how sympathetic pathways work to cause different outcomes.
FIGURE 20

A

pp. 82

NOTE: that sympathetic nervous system releases ACh causing vasodilation of vascular bed via M3-receptors in endothelial cells. (pp 84).

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12
Q

Show how B2-adrenergic receptor activation by NE results in Bronchiolar Smooth mm relaxation.
FIGURE 21

A

pp. 83

NOTE: B-adrenergic receptor activation usually causes relaxation of S mm.

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13
Q

Describe the physiological effects of alpha 1-adrenergic receptor activation.

A

Ca released via IP3 pathway, Ca-CaM complex activate MLCK (dephosphorylate it)-MLCK phosphorylate myosin light chain (MLC)-activating it and resulting in contraction.
-Constriction of large arteries, veins, arterioles-> decreased vascular compliance->increased central venous pressure->increased peripheral resistance->increased systolic and diastolic arterial pressure-> activate baroreceptor reflexes->bradycardia (inhibition of respiration)

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14
Q

T/F The parasympathetic system innervate vascular S mm.

A

F. Not involved in vascular S mm. But the sympathetic system indirectly induces cholinergic stimulation of blood vessels via the endothelial cells tht line the blood vessel lumen=>vasodilation
READ pp 84 (cholinergic) REFER to Fig. 20. pp83.

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15
Q

What is the notable exception to the general rule that alpha 1-adrenergic receptors cause S mm contraction?

A

S mm of the GI tract which relaxes when alpha 1-adrenergic receptors are activated.
-Occurs via increase in K permeability which causes hyperpolarization (precise method not known).

16
Q

How can B-stimulation treat asthma?

A

B-stimulation leads to dilation of the bronchial S mm important in treating asthma (Figure 21 pp 83).

17
Q

In general, what does the PS innervate when it comes to S mm? What receptors are mostly present?

A

PS innervate S mm other than those of blood vessels via the M3-cholinergic receptor and this results in mm contraction.

18
Q

How does M3 and M1 receptors cause peristalsis in the GI and bladder emptying?

A

M3 stimulation results in increase of Ca via IP3-> tone and amplitude of contraction increases, as well as peristalsis in the GI.
NOTE: M3 also enhances the secretory activity of GI but gastric acid secretion stimulated by M1-receptor activation

M1 stimulation is more important in the bladder. And via the same way with increase in Ca through IP3 cause bladder contraction and emptying.

19
Q

How does sympathetic nervous system activation affect the heart?

A

B1-adrenergic receptor activation->induce a cascade->cAMP increase->stimulate PKA-> phosphorylation of Ca channels=open at lower voltage and stay open longer—-depolarization at the SA node—faster HR.
NOTE: Pacemaker channels are rather directly stimulated by cAMP to shift activation curve of If to more +ve=the inward current is greater for every membrane potential.
STUDY Figure 22 pp 88

20
Q

What happens during exercise in terms of sympathetic stimulation?

A

-Sympathetic nervous system activation leads to
*phosphorylation of the If channel (within SA node)
*phosphorylation of Iks, L-type Ca channels in the ventricles
=Stronger and shorter AP

21
Q

How does the parasympathetic system affect HR?

A

PS stimulation decreases HR via
*inhibit adenylyl cyclase-decrease in cAMP
*Open K channels-hyperpolarization
=decreased HR

22
Q

How does the sympathetic nervous system affect the force of contraction of the cardiac myocytes?

A

B1-adrenergic receptor stimulation leads to PKA increase:

  • phosphorylation of L-type Ca channel +ve inotropic effect in both atria and ventricles-due to CICR and direct activation of contraction
  • Increased filling of SR with Ca due to increased intracellular Ca and increased pump activity (cAMP-dependent phsphorylation of phspholamban). This enhances fast relaxation.
  • Phosphorylation of Troponin I-reduces affinity of troponin C for Ca, allowing for more rapid dissociation of Ca from troponin-enhanced rate of relaxation.

FIGURE 23 pp88

23
Q

What is thought to cause the increased conduction velocity at the AV node due to sympathetic stimulation?

A

Greater opening of Ca channels.

24
Q

How does the parasympathetic system affect force of contraction of the cardiac myocytes?

A

M2 stimulation-
*opening of K channels-hyperpolarization of myocytes
*inhibit opening of L-Type Ca channels
*alpha i- subunit of Gi to adenylyl cyclase results in decrease cAMP
=negative inotropic effect

25
Q

Understand how sympathetic stimulation affect carbohydrate metabolism. FIGURE 24

A

pp. 90

26
Q

Fat lipolysis into free FA in the adipocytes is stimulated by_______

A

Beta 3-adrenergic receptors

27
Q

Explain how Beta 1-adrenergic stimulation activates phsphorylase kinase and inhibit the phosphatase in controlling glycogen metabolism.

A

-B1 adrenergic stimulation-phosphorylation (activation) of PKA-phosphorylation of glycogen phosphorylase-glycogen break down

-B1 adrenergic stimulation-phsphorylation of a phosphotase inhibitor ptn (activated)-binds to phosphatase and inhibits it
FIGURE 25 pp 93

28
Q

What does “sympathetic response provides an anticipatory response for SK mm activity (metabolism)” mean?

A

Phosphorylase kinase-multisubunit enzyme (1 catalytic, 3 regulatory).
-Calmodulin- regulatory subunit, Ca binding increase kinase activity
-Other 2 regulatory subunit modulated by cAMP-b/c phosphorylated by PKA-increase kinase activity
=> Increased intracellular Ca not only promotes contraction but also metabolically allow for sustained use.

29
Q

What is the dominant effect of epinephrine on insulin secretion?

A

Inhibit insulin secretion-net decrease in cAMP, results in smaller Ca influx through pancreatic B cells (alpha 2 adrenergic receptors)

NOTE: B2-stimulation leads to enhanced insulin secretion.

30
Q

What is the sympathetic effect on salivary and lacrimal glands?

A

Inhibit net secretion through reduced blood flow caused by vasoconstriction (alpha 1 and Beta receptors increase secretion but it is not significant and the net effect is inhibition).

31
Q

How are salivary glands affected by parasympathetic stimulation? FIGURE 27 95

A

M3 stimulation-increase in intracellular Ca opens 1) Ca activated K channels and 2) Ca activated Cl channels-both cations and anions move through channels and water flow follows.
*Rise in intracellular Ca also leads to ptn secretion via exocytosis.
NOTE: M3 activation stimulates sweating, BUT this is via sympathetic activation of the cholinergic receptors.

32
Q

How do sympathetic and parasympathetic innervation play important roles in the development and progression of cancer (Use prostate cancer as an example)?

A

The prostate gland receive both S & PS innervation.
-Cancer cells secrete substances that induce outgrowth-Ex. sympathetic adrenergic outgrowth-promote early case of cancer development.
-The parasympathetic release of ACh on stromal cells-invasion,migration, and metastasis of prostate cancer.
Figure 28 pp 96

33
Q

What is the difference b/n neurotransmitters and neuromodulators?

A

Neurotransmitters: directly causing a short term effect.
Neuromodulators: substances that modify neurotransmission.

34
Q

What are the receptors activated by ATP (adenosine)?

A

Purinergic receptors

35
Q

Which purinergic receptors do ATP and AMP preferentially act on?

A

ATP-P2 purinoreceptors- results in Ca increase via activation of Ca channels or opening of non-selective cation channels (NO second messengers)=> vasoconstriction. Act synergistically with the sympathetic NE stimulation of alpha 1
AMP-P1 purinoreceptors-works through the adenylyl cyclase to change level of cAMP

36
Q

What are some peptides secreted from autonomic nerves and modulate post synaptic events?

A

1) Substance P
2) Vasoactive Intestinal Peptide (VIP)
3) Somatostatin
4) Neuropeptide Y (NP Y)
- Have endocrine or neuroendocrine functions.
- Are neuromodulators.

37
Q

Mention 2 examples of how neuromdulators substance P and NPY work in sympathetic ganglia and arterial Smm respectively.

A

1) Substance P: excitatory effects are very slow in onset and have prolonged effects
2) NPY enhance vasoconstriction action of NE probably by inhibiting the opening of Ca activated K channels

CV Week 3 (8 decks)

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