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Second Year - Biomedical Sciences BS22001 > Lecture 30 - Pharmacology Of Smooth Muscle In Relation To Cardiovascular Function > Flashcards

Lecture 30 - Pharmacology Of Smooth Muscle In Relation To Cardiovascular Function Flashcards

1
Q

What constitutes most of the tunica media in blood vessels

A

Vascular smooth muscle (VSM)

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2
Q

What does vascular smooth muscle play an important role in

A

The control of vascular tone

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3
Q

What is a major regulator in the contraction in VSM

A

Calcium

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4
Q

How is calcium in vascular smooth muscle regulated

A

By an intricate system of calcium mobilisation and calcium homeostatic mechanisms

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5
Q

The interaction of a physiological agonist with its plasma membrane receptor stimulates

A

The hydrolysis of membrane phospholipids

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6
Q

Where is calcium released from

A

The sarcoplasmic reticulum

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7
Q

Where do agonists stimulate calcium release from

A

Extracellular space

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8
Q

What has to be stimulated by agonist to allow calcium release from the extracellular space

A

Voltage-gated, receptor-operated and store-operated channels

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9
Q

Calcium homeostatic mechanisms tend to

A

Decrease the intracellular free calcium concentration by activating calcium extrusion via the plasmental calcium pumps and the Na+/Ca2+ exchanger and the uptake of excess calcium by he sarcoplasmic reticulum and possibly the mitochondria

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10
Q

A threshold increase in the intracellular calcium concentration

A

Activates calcium-dependent myosin light chain phosphorylation, stimulates the actin-myosin interaction and initiates VSM contraction

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11
Q

What is nitric oxide (NO)

A

An endothelium-dependent vasodilator of the underlying smooth muscle

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12
Q

What does NO play a major role in

A

The maintenance of basal vasodilator tone of the blood vessels

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13
Q

How is NO formed

A

Under the influence of the enzyme nitric oxide synthase (NOS)

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14
Q

What is the action of NOS

A

It converts the amino acid L-arginine to NO

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15
Q

What produces NO in the vasculature

A

Endothelial NOS (eNOS)

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16
Q

What is inactive eNOS bound to

A

Caveolin

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17
Q

Where is inactive eNOS located

A

In the small invaginations in the cell membrane called caveolae

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18
Q

What happens to eNOS when intracellular levels of calcium rise

A

eNOS becomes detached from caveolin and is activated

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19
Q

NO agonists can influence

A

The detachment of eNOS from caveolin by releasing calcium from the endoplasmic reticulum

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20
Q

Examples of NO agonists

A

Bradykinin, acetylcholine, adenosine triphosphate, adenosine diphosphate, substance P and thrombin

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21
Q

Once intracellular calcium stores are depleted what happens

A

A signal is sent to the membrane receptors to open calcium channels allowing extracellular calcium into the cell

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22
Q

What is store-operated calcium entry of capacitive calcium entry

A

Once intracellular calcium stores are depleted a signal is sent to the membrane receptors to open calcium channels allowing extracellular calcium into the cell

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23
Q

What protein does calcium attach to

A

Calmodulin

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24
Q

Where is calmodulin found

A

In the cytoplasm of the cell

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25
Q

What happens after calcium is bound to calmodulin

A

It undergoes structural changes which allow it to eNOS

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26
Q

Once calcium is bound to eNOS what happens

A

eNOS converts L-arginine into NO

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27
Q

What does a reduction in calcium cause

A

The calcium-calmodulin complex to dissociate from eNOS, which in turn binds to caveolin and becomes inactive

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28
Q

What is the short term increase of NO dependent upon

A

The intracellular calcium

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29
Q

What is a mechanism to regulate NO production

A

Phosphorylation of eNOS

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30
Q

How does phosphorylation of eNOS occur

A

By the actions of protein kinases such as protein kinase A and cyclic guanosine-3’,5’-monophosphate (cGMP) protein kinase dependent II

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31
Q

What initiates eNOS phosphorylation

A

Sheer stress

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32
Q

The actions of what initiate eNOS phosphorylation through sheer stress

A

Protein kinase B (Akt)

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33
Q

What does sheer stress result from

A

Increased blood flow in the vessel

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34
Q

In what way can sheer stress induce NO production

A

eNOS phosphorylation and baby stimulating endothelial cell receptors by allowing the transfer of blood-borne agonist to attach to endothelial cell receptors and increase intracellular calcium

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35
Q

What does sheer stress activate in particular

A

Specialised calcium-activated potassium channels on the endothelial cell surfaces

36
Q

What does the activation of calcium-activated post assign channels cause

A

An efflux of potassium and an influx of calcium

37
Q

Once synthesised what happens to NO

A

It diffuses across the endothelial cell into the adjacent smooth muscle where it binds to the enzyme soluble guanyly cyclase (sGC)

38
Q

Once the enzyme sCG is activated what does it do

A

It increases the conversion rate of guanosine triphosphate to cGMP

39
Q

What does the present of cGMP do

A

It decreases smooth muscle tension, reduces calcium release from the sarcoplasmic reticulum and helps to restore calcium to the sarcoplasmic reticulum

40
Q

What do organic nitrate do

A

Relax all types of smooth muscle

41
Q

How to organic nitrates relax smooth muscle

A

By their metabolism to nitric oxide

42
Q

In small doses what effect do organic nitrates have on the body

A

They cause venorelaxation which decreases CVP, reduce SV, increased heart rate and there is no change in arterial pressure

43
Q

What effect do higher doses of organic nitrates have

A

They can cause arteriolar dilation which decreases arterial pressure, reducing the afterload

44
Q

What effect do organic nitrates have on coronary blood flow in normal subjects

A

The cause an increase in coronary blood flow

45
Q

What effect do organic nitrates have on angina patients

A

Blood is redirected towards the ischaemic zone

46
Q

What are the benefits of use in angine

A

Decreased myocardial oxygen requirements via decreased preload, decreased afterload and improved perfusion of the ischaemic zone

47
Q

What are the main types of organic nitrates used in angina

A

Glycerltrinitrate (GTN) and isosorbide mononitrate (ISMN)

48
Q

What are GNT and ISMN metabolised to

A

Nitric oxide

49
Q

Characteristics of GTN

A

It is short acting and undergoes first-pass metabolism

50
Q

How is GTN administered in stable angina

A

Sublingually or as a spray

51
Q

How is GTN administered in unstable angina

A

By IV

52
Q

How is GTN administered for a more sustained effect

A

By a transdermal patch

53
Q

Characteristics of ISMN

A

It is longer acting than GTN and is resistant to first-pass metabolism

54
Q

How is ISMN administered

A

Orally

55
Q

What is ISMN administered for

A

Prophylaxis and a more sustained effect

56
Q

What are adverse effects of organic nitrates

A

Headaches, hypotension, fainting, reflex tachycardia and formation of methaemoglobin

57
Q

How can reflex tachycardia be prevented

A

By the co-administration of a beta-blocker

58
Q

What do calcium antagonists block/prevent

A

The opening of L-type channels in excitable tissue in response depolarisation

59
Q

What does the blockage of L-type channels cause

A

A limit on the increase of the concentration of intracellular calcium

60
Q

What do L-type channels mediate

A

The upstroke of the AP in the SA and AV nodes and phase two of the ventricular AP

61
Q

What effect can calcium antagonists have on the AV node

A

They can reduce the rate and conduction through the node

62
Q

What effect do calcium antagonist have on contraction

A

They reduce the force of contraction

63
Q

What are the three main type of calcium channel antagonists

A

Verapamil, amplodipine and ditiazem

64
Q

What are the characteristics of verapamil

A

Relatively selective for cardiac L-type channels and blocks the pore

65
Q

Characteristics of amlodipine

A

It is a dihydropyridine compound which is relatively selective for smooth muscle L-type channels and acts allosterically to prevent channel opening

66
Q

When used to treat angina what effects do verapamil and diltiazem have

A

Negative inotropic effects

67
Q

What offsets the negative inotropic effects of verapamil and diltiazem

A

The baroreceptor reflex

68
Q

What are calcium antagonists used to treat

A

Hypertension

69
Q

What are the effects of calcium antagonists in hypertension

A

Reduce calcium entry into vascular smooth muscle which causes generalised arteriolar dilation causing a reduced TPR and MABP

70
Q

Example of a drug that is selective for smooth muscle L-type channels

A

Amloplipine

71
Q

What are adverse effects of calcium antagonists

A

Hypotension, dizziness, flushing and swollen ankles

72
Q

What is a dysthymia

A

An irregular heartbeat

73
Q

How is the ventricular rate in rapid atrial fibrillation reduced

A

By suppressing the conductance through the AV node

74
Q

What is normally used in rapid atrial fibrillation

A

Verapamil particularly in combination with beta-blockers

75
Q

Potassium channel openers open

A

ATP-modulated potassium (Katp) channels

76
Q

How do potassium channel openers act

A

By antagonising intracellular ATP which closes the Katp channel and causes hyperpolarisation which switches off L-type calcium channels

77
Q

What drug is used as a last resort in hypertension

A

Minoxidil

78
Q

What are the side effects of minoxidil

A

Reflex tachycardia and salt and water retention

79
Q

What is used in begins refactory

A

Nicorandil

80
Q

What are adrenoceptors

A

G-protein-coupled receptors (GPCRs)

81
Q

How are GPCRs activated

A

By the sympathetic transmitter noradrenaline and hormone adrenaline

82
Q

What do alpha1-adrenoceptors receptor antagonists cause

A

Vasodilation by blocking the vascular alpha1-adrenoceptor which causes a reduced sympathetic transmission which results in a decreased MABP

83
Q

What are the most frequency alpha1-adrenoceptor receptor antagonists

A

Prazosin and doxazosin

84
Q

What provide symptomatic relief in benign prostatic hyperplasia

A

Alpha1-adrenoceptor receptor antagonists

85
Q

What is benign prostatic hyperplasia

A

An abnormally enlarged prostate compressing the urethra

86
Q

What is the main adverse effect of alpha1-adrenoceptor receptor antagonists

A

Postural hypotension

Second Year - Biomedical Sciences BS22001 (28 decks)

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