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Pharmacology > How Drugs Affect the ANS > Flashcards

How Drugs Affect the ANS Flashcards

1
Q

Describe typical sympathetic pre- and post-ganglionic neurons

A

Pre-ganglionic: short axon

Post-ganglionic: long axon

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2
Q

NE alpha-1 receptors associate with what G-protein receptor? What is the end effect of this?

A

Gq; influx of intracellular Ca++

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3
Q

NE alpha 2 associates with what G-protein receptor; what is the end effect of this?

A

Gi; decreased voltage-gated Ca2+ channels

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4
Q

NE beta 1-3 receptors associate with what G-protein receptor; what is the end effect of this?

A

Gs; increases cAMP

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5
Q

What is the preferential molecule for alpha 1 receptors, NE or EPI?

A

NE

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6
Q

What is the preferential molecule for alpha 2 receptors, NE or EPI?

A

It is equal

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7
Q

What is the preferential molecule for B1 receptors, NE or EPI?

A

They are equal

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8
Q

What is the preferential molecule for Beta 3 receptors, EPI or NE?

A

EPI >> NE

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9
Q

Where is norepinephrine produced in the body and what is its precursor?

A

the presynaptic terminal of the neuron; tyrosine

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10
Q

What happens if you activate Gq in a smooth muscle cell?

A
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11
Q

What happens if you activate Gs in a smooth muscle cell?

A

Relaxation

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12
Q

What happens if you activate Gi in a smooth muscle cell?

A

Contraction

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13
Q

Under what circumstances might it be advisable to administer a beta agonist to the airway?

A

asthma

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14
Q

What happens if you activate Gs in a cardiac muscle cell?

A

Contraction

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15
Q

What happen if you activate Gi in a cardiac muscle cell?

A

Decreased contraction

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16
Q

Compare and contrast Gq signaling in smooth muscle vs. cardiac muscle

A

Gq signaling stimulates contraction in smooth muscle and has unconventional cardioprotective effects in cardiac muscle

17
Q

Compare and contrast Gs signaling in smooth muscle vs. cardiac muscle

A

Gs signaling stimulates relaxation in smooth muscle and contraction in cardiac muscle

18
Q

Compare and contrast Gi signaling in smooth muscle vs. cardiac muscle

A

Gi signaling stimulates contraction in smooth muscle and decreases contraction in cardiac muscle

19
Q

What happens if you activate Gi in a presynaptic terminal?

A
20
Q

Describe cardiac tissue response to sympathetic stimulation

A
  • Effects of EP and NE mediated primarily by B1 receptors
  • symp stimulation increases ALL aspects of cardiac fxn
    • SA node: incr rate (+ chronotropes)
    • Ventricles/atria: incr contractility (+ inotropes)
    • AV node: incr conduction velocity (+ dromotropes)
21
Q

Describe blood vessel tissue response to sympathetic stimulation

A
  • primary target: vascular smooth mm (VSM) cell
  • typically a pressor response (incr MAP)
    • alpha1 > VSM contraction > Incr resistance
    • beta2 > VSM relaxation > decr resistance
  • alpha effect predominates in most tissues
    • _​_except: sk mm, brain, large vv
22
Q

What is the cardiovascular response to NE?

A

Parasympathetic activation > rapid homeostatic mechanism to decrease heart rate and blood pressure (baroreceptor reflex) via the vagus nn.

23
Q

What is the eye tissue response to sympathetic stimulation?

A
  • alpha1 > contracts radial mm = mydriasis (pupil dilation)
  • beta2 > relaxes ciliary muscle = miosis (flattening of lens)
24
Q

What is the lung tissue response to sympathetic stimulation?

A
  • major effect = relaxation of bronchial smooth mm. via B2 receptor activation
  • regulation of bronchial glandular secretions is species-dependent and variable
    • beta2 > enhanced secretion
    • alpha1 > reduced secretion (predominates)
25
Q

What is the GI tract tissue response to sympathetic stimulation?

A
  • generally inhibited by increased sympathetic tone
    • beta2 > reduces motility by relaxing mm, reduces secretion
    • alpha1 > constricts sphincters
26
Q

What is the urinary bladder tissue response to sympathetic stimulation?

A
  • complimentary effects lead to reduced urination
    • alpha1 > constricts sphincter
27
Q

What is the sweat glands response to sympathetic stimulation?

A
  • symp postganglionic neurons are atypical as they are cholinergic (except in horses)
    • release ACh onto mAChR
    • horses exhibit “adrenergic sweating” (B2)

Pharmacology (33 decks)

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