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cardio exam 2 > Lec 34 Drugs acting on the ANS > Flashcards

Lec 34 Drugs acting on the ANS Flashcards

1
Q

What is the 1 synapse vs 2 synapse organization of our nervous system?

A

somatic uses 1 synapse

autonomic system uses 2 synapses = have preganglionic and postganglionic fiber

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2
Q

What are the 3 branches of the ANS?

A
  • parasympathetic
  • sympathetic
  • enteric
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3
Q

What is the action of enteric nervous system?

A
  • complex network of neruons in gut wall

mostly independent of CNS

does extensive intrinsic gut activity including peristalsis

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4
Q

Where are preganglion cell bodies located for sympathetic vs parasympathetic?

A

SNS: thoracic and lumbar levels of spinal cord

PNS: medulla, sacral levels of spinal cord

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5
Q

Which nerves cary preganglionic axons for SNS vs PNS

A

SNS: thoracolumbar = thoracic + lumbar

PSN: craniosacral = cranial and sacral

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6
Q

Where are ganglia located for SNS vs PNS?

A

SNS: near spinal cord in paravertebral or prevertebral ganglia

PNS: near or in wall of innervated organ

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7
Q

In what tissues do the SNS and PNS exert complementary/similar effects?

A

male sex organs

uterus during labor

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8
Q

What tissues are only innervated by one branch [PNS or SNS]?

A

vasculature = only SNS
liver = only SNS
sweat glands = only SNS

generally when something is innervated by only one branch its going to be sympathetic!

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9
Q

What types of ANS synapses release ACh?

A
  • all preganglionic neurons
  • all postganglionic PNS neurons
  • a few post-G SNS neurons = sweat glands
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10
Q

What types of ANS synapses release NE?

A

most sympathetic postganglionic neurons

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11
Q

What types of ANS synapses release dopamine?

A

sympathetic fibers that innervate the renal vasculature and some other vessel beds

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12
Q

What types of ANS synapses realease epinephrine?

A

not synaptic! its a hormone released by adrenal medulla

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13
Q

How can you tell wich is the predominant tone of a titssue?

A

usually its the branch of ANS that makes the organ or tissue contract/movie

ex. PNS increases GI motility so is dominant tone
exception: hearts predominant tone is PNS but PNS slows HR

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14
Q

How is ACh action terminated at synapse?

A
  • acetylcholinesterase [AChE] on postsynaptic membrane hydrolyzes
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15
Q

What is action of physotstigmine?

A

inhibits AChE –> more ACh around –> more PNS

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16
Q

How is action of catecholamines [NE, Epi, Dopamine] terminated at synapse?

A

mainly by reuptake of transmitter

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17
Q

What type of receptor is cholinergic nicotinic receptor? cholinergic muscarinic receptor?

A 
nicotinic = ionotropic = voltage gated
muscarinic = GPCR
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18
Q

How does nAChR of ANS ganglia differ from one at NMJ?

A

Nn = ganglionic type
Nm = NMJ type
different morphologies –> drugs can be selective for one type or the other

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19
Q

What are the different types of muscarinic ACh receptors? What G proteins are they coupled to?

A

M1/M3/M5 = couple to Gq
- activate phospholipase C, increase Ca, stimulate protein kinase C; mostly M3 in ANS

M2/M4 = couple to Gi and Go
- inhibit adenylyl cyclase and hyperpolarize membrane via GIRKs [inward rectifying K channels]; mainly M2 in ANS; activate G

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20
Q

What type of receptors are a receptors vs B receptors

A 
a = GPCRs
B = GPCRs
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21
Q

What are action of a1 vs a2 receptors? what G proteins?

A

a1 = expressed on possynaptic effector cells

  • couple to Gq –> IP3 and DAG –> elevate intracellular Ca and stimulate protein kinase C
  • contract smooth muscle in arterioles/viscera/pupils

a2 = inhibitory autoreceptors
- couple to Gi/Go –> reduce cAMP –> hyperpolarize membrane through activation of GIRK channels

22
Q

What are actions of B1/B2/B3 receptors? what G proteins?

A

all couple to Gs and increase cAMP

B1/B2 widely distributed

B3 expressed on fat cells and contribute to lypolysis

23
Q

Where are some tissues where B1 > B2 and some where B2 > B1?

A

B1> B2 in : heart, juxtaglomerular cels

B2 > B1 in: skeletal and coronary arterioles; bronchial smooth muscle;

24
Q

What are the 2 types of dopamine receptors in ANS? What G proteins?

A

D1 = couple to Gs –> mediate vasodilation; prominent in renal vasculature

D2 = couple to Gi –> negative feedback

25
Q

What is mech of action epinephrine? What does it do to HR, TPR, DBP, SBP, MAP at low dose?

A

non selective a and B receptor agonist

HR: increase
TPR: decrease slightly--> b/c more potent activity for B2 
DBP: decrease
SBP: increase
MAP: increase slightly
26
Q

What is mech of action norepinephrine? What does it do to HR, TPR, DBP, SBP, MAP at low dose?

A

selective a and B1 receptor agonist [no B2]

HR: decrease [b/c of baroreceptor reflex]
TPR: increase = b/c no B2 vasodilation
DBP: increase
SBP: increase
MAP: increase
27
Q

What is mech of action isoproterenol? What does it do to HR, TPR, DBP, SBP, MAP at low dose?

A

selective B receptor agonist

HR: increase a lot
TPR: decrease a lot = vasodilator
DBP: decrease a lot
SBP: decrease or slightly increase
MAP: decrease
28
Q

What are homeostatic mech on scale of sec? on scale of min to hr?

A

sec: autoreceptors sense recent history of transmiter release from terminal, inhibit more release

min/hrs: during periods of little synaptic activity, adiditonal receptors synthesized + placed in postsynaptic membrane [= denervation sensitization]; reverse occurs during period of high activity

29
Q

What is baroreceptor reflex?

A
  • decrease in BP sensed by baroreceptors
  • decrease baroreceptor activity conveyed to medulla
  • increased SNS and decreased PNS activity in medullary centers –> vasoconstriction and increase CO
  • homeostatic increase in BP
30
Q

What type of sympathetic receptors expressed in vasulature?

A
  • a1 receptors widely in vasculature

- B2 among vascular beds [in coronary + skeletal muscle arterioles]

31
Q

What is action of sympathetic acivity on vasculature?

A
  • net increase in TPR and decrease in venous capacitance

blood flow redistributed to vessels with lots of B2 and away from vessels where mostly a

renal blood flow preserved by activation of D1 receptors on afferent and efferent arterioles

32
Q

What is effect of sympathetic on the heart?

A

B1 receptors in ventricles; B2 in atria/ SA node

  • increase contractility via B1 [inotropy]
  • increase HR at SA node [chronotropy]
33
Q

What is role of GIRK current in SA node?

A

contributes to negative resting Vm

drives Vm toward Vk

34
Q

How is mechanism of sympathetic positive chronotropic effect?

A
  • stimulation B receptors increase intracellular cAMP
  • cAMP binds HCN [funny current] channels and increases their conductance
  • large If drives membrane voltage to AP spike threshold sooner
  • also acts to increase conudction velocity through AV node by increasing cAMP –> activates protein kinase A –> phsophorylate L type Ca channels and increases their conductance –> faster propagation
35
Q

What is mech of action of sympathetic on contractility/relaxation [positive inotropy/lusitropy]?

A
  • SERCA pump inhibited by phospholamban
  • cAMP activated PKA phosphorylated phospholamban –> high SERCA activity –> more Ca into SR –> more contractile strength
  • rate of relaxation following AP depends on how quickly SERCA can sequester Ca in the SR
36
Q

What are sympathomimemetic vs sympatholytic drugs?

A

sympathomimetic = direct agonists or uptake/degradation inhibitors or release; mimic effect of SNS NT release

sympatholytic = block normal sympathetic transmission = antagonists

37
Q

What is use of B-blockers?

A

have wide use in HTN, angina, arrhythmias, heart failure

use primarily in HTN due to excessive sympathetic activity; reduce mortality in CHF

38
Q

What is parasympathetic effect on vasculature?

A

few vessels PNS innervated so does not afect vascular tone

BUT there are muscarinic receptors on vascular endotehlium –> when activated release NO –> increase cGMP –> vasodilation

39
Q

What are parasympathetic effects on heart? mech?

A
  • mostly on atria
  • at SA node –> negative chronotropy

stimulate muscarinic receptors –> increase current through GIRK channels mediated by Gby –> membrane more negative between APs –> takes longer to reach spike threshold

at AV node –> negative dromotropy –> longer PR; AV block if too much

activates Gi–> reduce cAMP phosphorylation of Ca channels –> slow upstroke of AP

in atrial muscle –> decreased contractility and shorter AP duration by same mech

40
Q

What are PNS effects on airway?

A
  • bronchoconstriction

- increase secretions

41
Q

What are PNS effects on bladder?

A
  • contract bladder wall

- relax sphincter

42
Q

What are PNS effects on eye?

A
  • miosis

- near vision

43
Q

What are the types of cholinesterase inhibitors?

A
  • competitive inhibitors
  • carbamates
  • organophosphates
44
Q

What is SLUDGE signs of PNS overdose?

A
  • salivation
  • lacrimation
  • urination
  • defecation
  • GI pain
  • emesis
45
Q

What is killer B’s of PNS overdose?

A
  • bronchorrhea
  • bronchospasm
  • bradycardia
46
Q

What is DUMBELS of PNS overdose?

A
  • defecation
  • urination
  • miosis
  • bronchorrhea/bronchospasm/bradycardia
  • emesis
  • lacrimation
  • salivation
47
Q

What is use of carbamate and organophosphate type AChE inhibitors?

A

use as insecticides and nerve gases = sarin

48
Q

What is use of ganglion blockers?

A
  • antagonist of neuronal nicotinic receptors –> denervate autonomic targets = effect oppostie to predominant tone

–> HR increase; BP decrease

ANS reflexes absent when ganglia blocked

49
Q

What happens if you abruptly stop Beta blockers?

A
  • abrupt withdrawal can lead to exacerbation of angina and possible MI
  • need to taper off B blockers
50
Q

Who should you avoid giving beta blockers?

A

diabetes: give with precaution; can induce hypoglycemia and mask symptoms of hypoglycemia; also linked to increased risk of insulin resistance

avoid in pts with asthma b/c risk of bronchoconstriction

51
Q

What are adverse effects of beta blockers?

A
  • bradycardia
  • bronchoconstriction
  • fatigue
  • CNS effects
  • vasospasm –> worsening of raynaud’s phenomenon
  • erectile dysfunction

cardio exam 2 (19 decks)

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