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Pharmacology > Nervous and Hormonal Systems > Flashcards

Nervous and Hormonal Systems Flashcards

1
Q

how is the autonomic nervous system a good therapeutic target?

A

ANS neurons innervate almost all viscera
not protected by the blood brain barrier so drugs can easily interact
/ brain nerves are protected

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2
Q

what is a catecholamine?

A

A group of NT’s derived from tyrosine

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3
Q

what are the 3 main catecholamines?

A

dopamine, noradrenaline and adrenaline

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4
Q

what enzyme catalyses the first step in the conversion of tyrosine to adrenaline and NA?

A

tyrosine hydroxylase

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5
Q

what inhibits tyrosine hydroxylase?

A

end product inhibition from NA and a-methyl-tyrosine

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6
Q

what is a-methyl tyrosine used for?

A

inhibits catecholamines production e.g. NA/ adrenaline used to treat phaeochromocytoma

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7
Q

what is carbidopa used to treat?

A

inhibits DOPA decarboxylase, work in periphery not CNS, used in Parkinson’s disease in conjunction with L-Dopa, prevents unwanted effects of dopamine being produced in the peripheral nervous system

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8
Q

what is the mechanism of Methyldopa?

A

is taken up by sympathetic nerves and converted to α-methyl noradrenaline, it displaces NA from vesicles and when released has no effect it is a ‘false transmitter

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9
Q

what is methyldopa used to treat?

A

hypertension in pregnancy

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10
Q

where are Adrenaline and NA stored in the adrenal medulla?

A

chromaffin cells, in chromaffin granules

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11
Q

where are catecholamines stored in nerve terminals?

A

large dense-core vesicles ( 80nm diameter)
found in axons, cell body and varicosities
small dense- core vesicles (50nm diameter)
are found in varicosities only

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12
Q

what is the role of the VMAT?

A

vesicular monoamine transporter
antiport H+ / with NA or dopamine so it goes into the vesicle

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13
Q

what is the role of the ATP pump in vesicles in nerve terminals?

A

pumps in H+, keeps the PH low allows the antiporter activity of VMAT

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14
Q

where is dopamine converted to NA?

A

inside the vesicles in nerve terminals as well as maybe outside

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15
Q

what is the mechanism of reserpine?

A

inhibits VMAT, decrease catecholamines as they leak out and cannot be replaced?

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16
Q

what is reserpine used to treat?

A

used to treat hypertension but depression was a large side effect so mostly been withdrawn from use

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17
Q

what is the mechanism of action of clonidine?

A

α2-adreno receptor agonist, binds to pre junctional receptors on varicosities / nerve terminals to inhibit the release of NA

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18
Q

how is NA release controlled at the nerve terminals?

A

pre junctional receptors, activation either promotes of inhibits NA release
e.g. ATP / NA autoinhibit their own release from varicosities by binding to adrenoreceptors

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19
Q

how does parasympathetic nervous system inhibit sympathetic nerves?

A

lateral inhibition Ach released from parasympathetic nerve terminals bind to pre junctional muscarinic receptors to inhibit NA release

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20
Q

how does adenosine inhibit NA release

A

adenosine inhibits release via A1 receptors (comes from ATP broken down in the extracellular space)

21
Q

explain the autonomic side effect of opioids such as morphine?

A

inhibit release via ɥ-receptors e.g. morphine is a potent analgesic which inhibits NA release via prejunctional receptors
= dilated pupils / constipation

22
Q

what are the neuronal uptakes of catecholamines?

A

secondary noradrenaline transporter (NAT), cotransports (symporter) Na, Cl and catecholamines

23
Q

what are the non- neuronal uptakers of catecholamines?

A

done by a different NAT, in smooth muscle / cardiac / endothelium cells
low affinity (not very selective e.g. also uptakes adrenaline)
high max capacity

24
Q

explain the mechanism of action of cocaine

A

acts on many catecholamines transporters to inhibit their reuptake e.g.
NAT, SERT, and DAT, this increases dopamine and serotonin in the synaptic cleft leading to euphoria and excitement
side effect cause by inhibition of NAT = excess in the cleft = excess sympathetic activation

25
Q

what are the non - neuronal uptake channels of NA inhibited by?

A

normetanephrine (metabolite of NA) steroid hormones phenoxybenzamine

26
Q

what are the 2 main enzymes involved in the early stages of catecholamine metabolism?

A
  • Monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT)
27
Q

what enzymes 2 enzymes are involved in later stages? what nervous system to they mainly act on?

A

aldehyde dehydrogenase (ADH), mainly in the periphery and aldehyde reductase (AR), mainly in the CNS

28
Q

where is MAO found?

A

bound to Mt membrane in many tissues including neuronal

29
Q

What drug inhibits MAO?

A

phenelzine, leading to an increased level of dopamine 5-HT and NA in brain and peripheral tissues

30
Q

what are the side effects of drugs that inhibit MAO?

A

postural hypertension, atropine like effects, weight gain and insomnia

31
Q

where is COMT found and how does it act?

A

COMT is cytoplasmic and found in many tissues including nerve terminals, Converts catecholamines to methoxy derivatives by transferring a methyl group (from S-adenosylmethionine) to one of the catechol -OH groups
Acts not only on catecholamines, but also on the products of other degradative reactions (MAO, ADH, AR)

32
Q

explain the action of Noradrenergic Neuron Blocking Drugs

A

taken up into the nerve terminal and inhibit the firing of action potentials by interacting with ion channels

33
Q

give an example of a Noradrenergic Neuron Blocking Drugs

A

bretylium

34
Q

why are Noradrenergic Neuron Blocking Drugs not commonly used?

A

severe side effects of postural hypotension, diarrhoea and failure of ejaculation

35
Q

what is an indirectly acting sympathetic amine?

A

structurally related to catecholamines and can enter into neurons where they are up taken and displace the NT increasing the amount in the synaptic cleft?

36
Q

give examples of Indirectly Acting Sympathetic Amines

A

amphetamine (speed) and ephedrine (nasal decongestant)
increases levels of dopamine and 5H-T

37
Q

what are the side effects of amphetamine?

A

Long lasting effects on body include increased BP, bronchodilation, vasoconstriction

38
Q

what is the general structure of adrenoreceptors?

A

G protein coupled receptors, with Single polypeptide chain: 400 - 500 amino acids, Extracellular N-terminus, intracellular C-terminus, 7 transmembrane a helices

39
Q

where is the binding site for adrenoreceptors?

A

Binding site buried within a cleft between the α helices

40
Q

what is the binding site for the G protein in adrenoreceptors?

A

Experiments have determined that it is the long 3rd cytoplasmic loop that couples to the G protein, between α and β adrenoreceptors the amino acid sequence is different, this results in them coupling to different G proteins

41
Q

what is the mechanism of A1 adrenoreceptors?

A

NA binds, recruits Gq protein, activates phospholipase C
(Cleaves PIP2 into IP3 and DAG)
IP3 binds to receptors on rough ER increasing intracellular calcium levels
DAG, causes other effects mainly via PKG

42
Q

where are A1 adrenoreceptors commonly found?

A

smooth muscle on blood vessels

43
Q

give an example of where A2 adrenoreceptors are commonly found?

A

pre-junctional receptors on nerve terminals that when activated reduce release of catecholamines

44
Q

explain the mechanism of A2 adrenoreceptors?

A

Gi protein activated, inhibits adenyl cyclase, decreases cAMP
decreases activation and phosphorylation activity of PKA, reduces phosphorylation of proteins (e.g. those needed for NT release)

45
Q

explain the mechanism of B adrenoreceptors?

A

All B receptors use the same G protein Gs, they do the exact opposite of α2 receptors
It stimulates adenyl cyclase to act, increasing cAMP and phosphorylation of proteins by PKA
e.g. of MLCK causing vasodilation

46
Q

give an example of a A2 adrenoreceptors agonist

A

clonidine, binds to prejunctional, A2, decrease catecholamine, release used to treat hypertension

47
Q

give an example of B2 receptor agonist?

A

salbutamol, asthma causes bronchodilation

48
Q

what are the adverse effects of B adrenoreceptor antagonists?

A

bronchoconstriction (don’t give to asthmatics)
worsening of pre existing cardiac failure
bradycardia

Pharmacology (7 decks)

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