Exam #1: Physiology of the ANS II Flashcards Preview

Medical Physiology > Exam #1: Physiology of the ANS II > Flashcards

Flashcards in Exam #1: Physiology of the ANS II Deck (63):
1

What muscarinic receptors are present in the heart? What nervous system are they associated with?

- M2
- PNS

2

What type of G-protein is associated with the M2 receptor in the heart?

Gi/o= inhibitory G-protein

Decrease cAMP & PKA

3

What do M2 receptors inhibit in the heart?

- SA node= negative chronotrope
- AV node= decreased conduction velocity
-Atrial muscle= decreased atrial contracion
- Ventricular muscle= decreased ventricular contracion

4

What type of muscarinic receptor is present in the lungs?

M3

5

What is the effect of M3 activation in the lungs?

- Contraction of the bonchi & bronchioles
- Secretion from submucosal glands

*DO NOT use drugs in asthma patients that have PNS activity

6

What type of muscarinic receptor is present in the stomach? What is the effect of stimulation of these receptors?

M3, motility & cramps

7

What type of muscarinic receptor is present in the glands? What is the effect of stimulation of these receptors?

M1, secretion

8

What type of muscarinic receptor is present in the intestine? What is the effect of stimulation of these receptors?

M3, contraction--diarrhea & involuntary defecation

9

What is the general clinical picture of ACE inhibitor intoxication?

Voiding, urinary incontinence

V. wet

10

What is the difference between a coupled cell & an indirectly coupled cell?

- Directly coupled= directly activated by a neurotransmitter released from a varicosity
- Coupled= junction potentials spread from directly innervated cells
- Indirectly coupled= a sufficient area of a muscle bundle is depolarized to propagate the action potential to the cell

11

What does the innervation of the visceral smooth muscle differ from the vascular smooth muscle?

Visceral smooth muscle receives input from one source.

Vascular smooth muscle receives input from 2x sources:
1) Perivascular nerves
2) Endothelial input

12

What effects are mediated by perivascular nerves?

- A number of neurotransmitters released from varicosities in the tunica adventita act on receptors in the media, leading to vasoconstriction.

13

What effects are mediated by endothelial input?

- In response to shear stress or hypoxia, endothelial cells release factors that mediate vasodilation (Endothelium-Derived Relaxing Factors)

14

What is the effect of damage to the endothelial cell layer?

- When the Endothelium is damaged, activation of M3R on vascular smooth muscle causes vasocontriction (unopposed by EDRFs)

15

Outline the pathway that underscores the effects of M3R activation in the blood vessels.

1) ACh binds to M3
2) Increase intracellular Ca++
3) Increase in Nitric Oxide Synthase
4) Increased NO production via the endothelial cell
5) Relaxation

16

Why is vasoconstriction the outcome if the endothelium has been damaged?

Ca++ increase leads to contraction of the smooth muscle, but there is not the opposing NO, ultimately resulting in vasoconstriction.

17

Describe the mechanism of M1 & M3 receptor activation.

1) Receptor activation
2) Gq (activation)
3) PLC
4) PIP2-->IP3 & DAG
5) Increase Ca++ & PKC

18

Describe the mechanism of M2 receptor activation.

1) Receptor activation
2) Gi
3) Adenylul Cyclase inhibited
4) Decrease cAMP
5) Decrease PKA

19

Name the three locations of nicotinic ACh receptors.

1) PNS ganglia
2) Targets of the somatic nervous system, skeletal muscle
3) Adrenal medulla

20

What type of nicotinic receptor is present in the adrenal medulla? What is the response to ACh binding?

- Nn
- Secretion of Epi & NE

21

What type of nicotinic receptor is present in the autonomic ganglia? What is the response to ACh binding?

- Nn
- Stimulation

*Note that all autonomic ganglia have nicotinic AChR

22

What type of nicotinic receptor is present in the neuromuscular junction? What is the response to ACh binding?

- Nm
- Stimulation i.e. twitch & hyperactivity of skeletal muscle

*Remember skeletal MUSCLE, N-M*

23

How are catecholamines synthesized?

1) Tyrosine is converted to DOPA via Tyrosine Hydroxylase*
2) DOPA is converted to Dopamine
3) Dopamine is converted to Norepinephrine

*Note that this is the rate-limiting step*

24

What drug blocks tyrosine hydroxylase? What step of the catecholamine synthesis process does this drug block?

- Metyrosine
- Conversion of Tyrosine to DOPA

25

What part of catecholamine synthesis only occurs in the adrenal medulla?

Norepinephrine is converted to Epinephrine

26

What is tyramine?

Tyramine is a naturally occurring monoamine compound, and a trace amine derived from the metabolism of tyrosine (alternative to DOPA)

27

What causes an increase in Tyramine?

Ingested of naturally occurring fermented cheese

28

What is Tyramine a precursor of?

Norephinephrine

29

How are catecholamines stored?

Synthesized catecholamines are transported into vesicles for storage via the "Vesicular Monoamine Transporter (VMAT)"

*Note that the conversion of norephinephrine to epinephrine occurs in the vesicle, if the converting enzyme is available.

30

What blocks VMAT? What is the mechanism of action?

Reserprine, blocks VMAT & causes a depletion of catecholamine stores

*Still used today for "resistant hypertension*

31

How are the catecholamines released?

Similar exocytosis mechanism as ACh

32

What drug blocks VAMP?

Bretylium

33

How is catecholamine transmission terminated?

1) Diffusion into the circulation & metabolized by liver COMT (catechol-O-methyl transferase)
2) Binding to an autoreceptor on the pre-synaptic nerve terminal
3) Neuronal Re-uptake via NET1 (NE transporter on the presynaptic nerve terminal), where:
- Repackaged in vesicles
- Metabolized by mitochondiral monoamine oxidase (MAO)
4) Extraneuronal uptake via extraneuronal transporters (ENT or NET2)

34

What is the mechanism of action of cocaine & tricyclic antidepressants?

NET1 antagnoists that leads to an increase in NE in the synaptic cleft

35

What is the effect of MAO antagonists? How are they related to Tyramine?

MAO is a mitochondrial enzyme that metabolizes catecholamines
- Irreversible MAO antagonists enhance the availability of Tyramine
- Can lead to hypertensive crisis

36

Where are alpha-1 receptors located?

Vascular smooth muscle

37

Describe the mechanism of alpha-1 receptor activation.

1) Catecholamine binding to alpha-1 receptors leads to simulation
2) Gq subunit activated
3) Gq activates PLC
4) PLC leds the the release of IP3 & DAG
5) IP3 stimulates the release of sequestered Ca++
6) Ca++ then activates Ca++ dependent protein kinases

38

Describe the mechanism of B1 & B2 activation.

1) Catecholamine binding to B1 or B2 receptor leads to stimulation
2) Gs subunit activated
3) Activation of adenlyl cyclase
4) Increased cAMP
5) Increase PKA

39

Describe the mechanism of alpha-2 activation.

1) Catecholamine binding to alpha-2 receptor
2) Gi subunit activated
3) Inactivation of adenlyl cyclase
4) Decrease cAMP
5) Decrease PKA

40

Where are alpha 1 receptors located in the eye?

Radial (dilator muscle)

41

Where are B1 receptors located in the eye?

Ciliary body epithelium

42

Where are B2 receptors located in the eye?

Ciliary muscle
Ciliary body epithelium

43

What is the effect of stimulating alpha 1 receptors in the eye?

- Alpha-1 receptors are associated with the radial (dilator) muscle
- Contraction of the muscle results in dilation/ mydriasis

44

What is the effect of stimulating B1 receptors in the eye?

- B1Rs are associated with the ciliary body epithelium
- Increased production of aqueous humor?

45

What is the effect of stimulating B2 receptors in the eye?

- B2Rs are associated with the ciliary body epithelium &ciliary muscle
- Constriction & increased production of aqueus humor?

46

What is the effect of stimulating alpha 1 receptors in the arterioles?

Contraction of the smooth muscle leading to an increase in total peripheral resistance, diastolic pressure, & afterload

47

What is the effect of stimulating alpha 1 receptors in the veins?

Contraction of the smooth muscle leading to an increase in venous return & an increase in preload

48

What is the effect of stimulating alpha 1 receptors in the liver?

An increase in glycogenolysis

49

What is the effect of stimulating alpha 1 receptors in the male sex organs?

Ejaculation

50

What is the effect of stimulating alpha 1 receptors in the bladder & internal sphincter?

Contraction & urinary retention

51

What is the effect of stimulating alpha-2 receptors in the platelets?

Aggregation

52

What is the effect of stimulating alpha-2 receptors in the pancreas?

Decreased insulin secretion

53

Where are B1 receptors located?

Heart
- SA Node
- AV Node
- Atrial & Ventricular Muscle
- His Purkinje
Kidney

54

What is the effect of B1 receptor activation in the heart?

SA Node= positive chronotrope
AV Node= positive dromotrope
Atrial & Ventricular M.= positive ionotrope

?

55

What is the effect of B1 receptor activation in the kidney?

Increased renin release

56

Where are B2 receptors located?

Blood vessels
Uterus
Bronchioles
Skeletal Muscle
Liver
Pancreas

57

What is the effect of B2 receptor activation in the blood vessels?

Vasodilation leading to a decrease in total peripheral resistance, diastolic blood pressure, & afterload

58

What is the effect of B2 receptor activation in the uterus?

Relaxation

59

What is the effect of B2 receptor activation in the bronchioles?

Dilation

60

What is the effect of B2 receptor activation in the skeletal muscle?

- Glycogenoylsis
- Contractility/ tremor

61

What is the effect of B2 receptor activation in the liver?

Glycogenolysis

62

What is the effect of B2 receptor activation in the pancreas?

Insulin secretion

63

What is the rate-limiting step in catecholamine synthesis?

Conversion of Tyrosine to DOPA via Tyrosine Hydroxylase

Decks in Medical Physiology Class (74):