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Final Test: Dynamics II > Introduction to Autonomic Pharmacology part 2 > Flashcards

Introduction to Autonomic Pharmacology part 2 Flashcards

1
Q

What happens to the NE that is taken back into the cell

A

its repackaged into vessicles by the vescular monoamine transporter

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2
Q

What is MAO and COMT

A

MAO is know as monoamine oxidase

COMT is known as catechol-O-methyltransferase

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3
Q

What does MAO do

A

deaminate NE, Epi, and dopamine

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4
Q

Where is MAO located and what is its form

A

its located on the outer surface of the mitochondria

it has two forms: A and b

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5
Q

If MAO is inhibited what happens

A

inhibitiors elevate levels of the neurotransmitters in the synapse and are useful in treating depression, Parkinson’s disease and other CNS diseas

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6
Q

What is COMT and where is it located

A

an enzyme, its found in the cytoplasm of the liver cells and is involved in the metabolism of endogenous circulation and administed catecholamines by O-methylation reaction

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7
Q

What is the function of COMT

A

its involved in the metabolism of endogenous circulating and administered catecholamines by O-methylation reaction

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8
Q

What is the mechanism of transmitter release

A
  1. the priniciple way is exocytosis– the neutrotransmitter is stored in intracellular vesicles
  2. vesicles fuse transiently with cell membrane and discharge their contents, in response to increase in intracellular Ca2+ concentrations
  3. monoamine transmitters leak out by carrier mediated transport as well as NO and a.a. metabolites can diffuse
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9
Q

What are parasypathetic and sympathetic nerve varicosities

A

in the autonomic nervous system—long thin axons that are branched and have small enlargements or varicosities

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10
Q

What is the function of varicosities

A

neurotransmitter is synthesized and stored in caricosities- 20,000 per neuron and release the transmitters into the extracellular space

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11
Q

What happens to neurotransmitters after they are released from varicosities

A

they diffuse through extracellular space and affect many effector tissues cells: one neurone is capable of innervating an entire organ

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12
Q

What is non-adrenergic non-cholinergic transmission

A

that autonomic transmision can not be completely blocked by drugs that abolish response to NE or Epi because there are many other mediator secreted

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13
Q

How was it determined that there were more transmitters than NE and Epi

A

by fluorescence and immunocytochemical methods

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14
Q

What are the most common transmitter substance; but what are the other kinds

A

peptide are the most common transmitter substance but ATP and purines are also present; neurons contains as many as five different possible transmitters

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15
Q

What is the most extensively studied system containing NANC neurons

A

the enteric system in the gut wall ( in addition to cholineric and adrenergic fibers)

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16
Q

What is the rule of NANC transmission

A

co-transmission is the rule rather than the exception–release of more than one neurontransmitter from the same neuron

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17
Q

What is the location and function of neuropeptide Y, ATP, Dopamine, Enkephalin and related opoid peptide

A

*neuropeptide Y–

location: secretomotor neurons in the ENS

function:

1) inhibit the secretion of water and electrolyytes by the gut
2) causes long lasting vasconstriction
3) cotransmitter in many parasympathetic postganglionic neurons
4) sympathetic postganglionic noradrenergic vascular neurons

*ATP (adenosine triphosphate)—

location: cotransmitter at inhibitory ENS neuromuscular junctions

function:

1) inhibits release ACh and norepinephrine from ANS nerve endings
2) excitatory transmitter in the nerves of the vas deferens

*Dopamine

location: important postganglionic sympathetic transmitter in renal blood vessels

function:

1) a modulatory transmitter in some ganglia and the ENS

*Enkephalin and related opoid peptide

location: some secretomotor and interneuron in the ENS
function:
1) inhibit the ACh release and thereby inhibit peristalsis; may stimulate secretion

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18
Q

What is the location and function of galanin, CCK, CGRP, GABA, GRP, and NO

A

–Galanin:

Location: present in secretomotor neuron

Function: may play a role in appetit-saitety mechanisms

–Cholecystokinin

Function: acts as a cotransmitter in some excitatory neuromusclar ENS neurons

—Calcitonin gene related peptide (CGRP)

Location: in the substance P in cardiovascular sensory nerve fibers, some secretomotor ENS neurons and interneurons

Function: a cardiac stimulant

—GABA ( gamma-aminobutyric acid)

Function:

1) presynaptic effects on excitatory ENS nerve terminals (not a major transmitter in the ENS)
2) relaxant effect on the gut

—gastrin releasing peptide (GRP)

Function: extremely potent excitatory transmitter to gastrin cells; known as mammalian bombesin

—NO (nitric oxide)

Function: co-transmitter at inhibitory ENS neuromuscular junction; important at sphincters

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19
Q

What is the location and function of 5-HT, substance P, and VIP

A

5-HT (Serotonin)::

Function: co-transmitter at inhibitor ENS neuromuscular junctions; important at sphincters

Substance P (and related “tachykinins)::

Location: an important sensory neuron transmitter in the ENS and elsewhere

Location: CGRP in cardioivacular sensory neurons

“tachykinins”- excitaory cotransmitters with ACh at ENS neuromuscular junctions

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20
Q

What is neuromodulation of synaptic transmisssion

A

its control of transmission of different levels such as autoreceptors and heteroreceptors

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21
Q

What are autoreceptors and how do they work

A

neurotransmitters may act upon autoreceptors present on the presynaptic terminal to modulate its own release and uptake process

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22
Q

What are heteroreceptors and how do they work

A

its a receptor regulating the synthesis and/or release of mediator other than its own ligand.

for example a2 receptors found presynaptically on cholinergic neurons activation by NE results in inhibition of ACh release

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23
Q

How do the autoreceptors on cholinergic neurons work

A

heteroreceptors–the cholinergic neuron which releases ACh has an alpha-2 sympathetic receptor

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24
Q

How does the receptor modulate the release of neurotransmitters

A
25
Q

What is another way to modulate synaptic transmission

A

by altering ion currents either hyperpolarize (elevate threshold) or depolarize (decrease threshold) of the axon terminal

Of activation of second messenger systems such as cAMP or cGMP can lead to phosphorylation of various protein involved in the activity of the acon terminal such as transporters and vesicle proteins

26
Q

Explain the schema of presynaptic autoreceptors

A

regulate neurotransmitter release in adrenergic (release NE) and cholinergic neurons (ACh)

                                                                                                                                                                                                                             A2 and B2- adrenergic receptors exist on post sympathetic nerve terminal and inhibit the release of the neurotransmitter, NE

Muscarinic and nicotinic cholinergic receptors exist on postganglionic parasympathetic neuron that block release ACh. A2 adrenergic receptors also exist cholinergic neurons and inhibit Ach release–for

adrenergic neurons (those that release neurotransmitters that go to adrenergic receptors)–NE

cholinergic neurons (those that release neurotransmitters that go to cholinergic receptors)–ACh

27
Q

What are the two main types of Ach receptors

A

muscarinic and nicotinic receptors

28
Q

What is the alkaloid muscarine and where does it work; how is the name muscarine receptors fitting

A

the poisonous agent in toadstools-Amanita muscaria- they have little to no effect on receptors in autonomic gangia but mimics the action of ACh on the effector of smooth muscle

therefore the actions of ACh on SM effector organs and on heart muscle are known as muscarinic and the receptors are know as muscarinic receptors

29
Q

What are cholinergic receptors

A

these are the ACh receptors can be divided into two main types: muscarinic and nicotinic receptors

30
Q

Why is the name nicotinic receptors fitting and how does blocking muscarinic receptors help

A

in the autonomic ganglia, the actions of ACh can be reproduced by the drug nicotine. The actions of ACh in sympathetic ganglia are referred to as nicotinic, the receptors are known as nicotinic receptors

by blocking the muscarinic effects and then larger doses of ACh produce nicotinic effects. In addition with ganglionic effects, stimulation of voluntary muscle and simulation of Epi secretion from the adrenal medulla is also observed

31
Q

What are the effects of Ach on nicotinic receptors

A

nicotinic receptors are located where quicker responses are needed (adrenal gland)

found in sympathetic and parasympathetic postganglionic neurons at neuromuscular junctions of skeletal muscles, and at some cholinergic synapses in the central nervous system

32
Q

What type of effects was seen with acetylcholine on the cat’’s blood pressure

A

ACh causes a fall in blood pressure due to vasodilation, larger doses produce bradycardia—these are muscarinic effects

33
Q

What are the two types of cholinergic receptors

A

nicotinic and muscarinic

34
Q

What are the nicotinic receptors and what is their neutrotrasmitter

A

nicotinic ACh receptors are ligand-gated ion channels that are composed of multiple subunits (a pentamer w/’ 1-4 distinict subunits–subunits around an internal channel)

35
Q

How do nicotinic receptors work, describe using the diagram

A

two ACh molecules bind to the receptor to cause the Na+ channel to open

the Na+ increase with the cell, an action potential is generated leading to a response

36
Q

What are the two subtypes of nicotinic receptors

A

two subtypes of nicotinic receptors:

1) Nm found @ sketeletal muscle and neuromuscular junction
2) Nn which is neuronal subtype (ganglia and adrenal gland)

37
Q

What are muscarinic receptors and what is their neurotransmitter

A

G-protein coupled receptors that exhibit classical 7 transmembrane topology and activates second messengers

38
Q

What are the five muscarinic receptor subtypes

A

M1-M5 subtypes of muscarinic receptors

39
Q

How do M1, M3, M5 work (odd numbers)

A

the M1, M3, M5 are coupled to the stimulation of IP3/ DAG pathway via Gq

40
Q

How do M2 and M4 work (even numbers) and what is imporatant about M2 receptors

A

M2 and M4 are coupled to inhibition of cAMO production via an inhibitory G-protein

M2 receptors are coupled to elevation of K+ excretion which lead of hyperpolarization via a G-protein

41
Q

What is the difference between nicotinic and muscarinic receptors; which is slower and what is this important

A

the difference is their speed of action; nicotinic receptors produces almost instantaneous responses and muscarinic receptors results in slower but more prolonged effects (why muscarinic receptors results in slower but more prolonged effects

42
Q

Summarize the location and function of nicotinic receptors

A

nicotinic receptors are located where quicker responses are needed (adrenal gland); nicotinic receptors are found in sympathetic and parasympathetic postganglion neurons, at neuromuscular junctions of skeletal muscles, and at some cholinergic synapses in the central nervous systems

43
Q

Summarize the location and function of muscarinic receptors

A

found primarily in the membranes of visceral effectors, example in the heart, gastro-intestinal track, arterioles of genitalia, iris of the eye, salivary and sweat glands, lungs airways and urinary bladder

44
Q

Or rare occasion what can Ach interact with what receptors

A

although the primary receptors at the ganglia is nicotinic can have M1 receptors; ACh interacts with Nm receptors but on rare occasions can interact with minor M1 (muscarinic) receptors

45
Q

What are the adrenergic receptors

A

receptors where epinephrine, norepinephrine, isoproteranol work on; a multitude of subfamilies and subtypes of adrenergic receptors have been identified, alquist made the first differentiation of subfamilies

46
Q

What is the order of the adrenergic agonist

A

potency of adrenergic agonists in the stimulation of smooth muscle contration in vasculature was:

epinephrine> norepinephrine> isoproteranol (alpha receptor mediated)

for the same agonist, the rank order of potency for stimulation of heart rate was:

isoproteranol> epinephrine> norepinephrine (beta receptor mediated)

47
Q

What is the rank order of potency for stimulation of heart rate

A

isoproteranol> epinephrine> norepinephrine

its beta receptor mediated

48
Q

How is the response of the vasculature classified compared to the heart

A

its classified as alpha-receptor mediated

49
Q

What molecular tool allowed for classification of alpha and beta receptors

A

advent of more selective compounds and the tools of molecular biology have greatly expanded these obeservation of alpha and beta receptor mediated–and even more specific sub-classification of alpha and beta receptors

50
Q

How do the adrenergic receptors work

A

all adrenergic receptors are G-protein coupled and therefor activate second messengers but they differ in which second messengar they activtate, their tissue distrbution, DNA sequence and their pharmacological profile

51
Q

How are beta adrenergic receptors classified

A

classified into three subtypes: beta1, beta2, and beta3

all three subtypes are coupled to the activation of cAMP via Gs—> cAMP the activates protein kinase A which can phosphorylate various proteins to either activate or inhibit them

52
Q

What is the activation of beta-adrenergic receptors coupled to?.

A

activation of cAMP via Gs

53
Q

Compare the sensitivity of alpha receptors and beta receptors to which neurotransmitter

A

alpha receptors stimulated mostly by NE

beta receptors more sensitive to epinephrine

54
Q

What is the rule if alpha and beta receptors are both present; give an example

A

Rule: if alpha and beta receptors are present

alpha= excitation

beta= inhibition

For example, in skeletal muscle’s arterioles, norepinephrine secreted by post-ganglionic neurons—> vasoconstriction by alpha receptors (excitation)

beta-2 receptors stimulated by circulating Epi—> vasodilation (inhibition)

55
Q

What is an exception of the beta and alpha receptor rule

A

exceptions: beta-1 receptors stimulate heart to beat faster and stronger contraction; muscarinic-2-receptors decrease strength of contraction

56
Q

What are types of the alpha adrenergic receptors

A

alpha-1 and apha-2

57
Q

What are the subtypes for alpha-1- receptor and how do the pathways waork

A

there are 3 subtypes of alpha 1 receptors: 1A, 1B, 1D all of which are coupled to the activation of IP3 / DAG pathway—> DAG can activate PKC and subsequent protein phosphorylation—-> IP3 can elevate intracellular Ca2+ level

58
Q

What are the subtypes for alpha-2-receptors and how do the pathways work

A

there are 3 subtypes of alpha receptors: 2A, 2B, and 2D

2A and 2B decrease intracellular Ca2+ levels

2A elevates K+ conductance (hyperpolarizing)

59
Q

Explain ocular pharmacology

A

Final Test: Dynamics II (11 decks)

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