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Cardiovascular Pharmacology > Control of Vascular Smooth Muscle > Flashcards

Control of Vascular Smooth Muscle Flashcards

1
Q

What are the regulatory mechanisms of vascular smooth muscle?

A

ANS

Endothelium

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2
Q

What are the layers of the endothelium of the vasculature?

A

tunica externa
tunica media
tunica intima

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3
Q

what is the tunica externa?

A

loose connective tissue keeping the vessel together

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4
Q

What is the tunica media?

A

smooth muscle

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5
Q

What is the tunica intima?

A

endothelial cells lining the vasculature

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6
Q

What are the features of arteries?

A

large lumen to facilitate flow
lots of muscle
conduit of blood

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7
Q

What are the features of veins?

A

limited smooth muscle
60% of the blood when body at rest
capacitors

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8
Q

What are the features of arterioles?

A

high resistance

fine regulators of blood perfusion

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9
Q

What are the features of capillaries?

A

no smooth muscle
single layer of epithelium
can’t contract or dilate

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10
Q

What is the approximate BP of capillaries?

A

2mmHg

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11
Q

How is the amount of blood in the capillary bed regulated?

A

the precapillary sphincter muscles and small artery and arteriolar resistance

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12
Q

What maintains unidirectional flow in veins?

A

venous valves

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13
Q

How may drugs influence the blood flow and vessels?

A

antagonising, blocking, inhibiting endogenous proteins or activating the endogenous proteins

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14
Q

Give an example of drugs that may interact with cell surface receptors

A

Angiotensin receptor blockers - Losartan

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15
Q

Give an example of drugs that antagonise nuclear receptors

A

mineralocortocoids receptor antagonist - spironolactone

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16
Q

Give an example of drugs that inhibit enzymes

A

ACE inhibitors - ramipril

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17
Q

Give an example of drugs that inhibit ion channels

A

Na Channel Blockers - lidocaine

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18
Q

Give an example of drugs that inhibit transporters

A

inhibitors of Na-K-2Cl symporter i.e. loop diuretics - furosemide

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19
Q

Give an example of drugs that inhibit signal transduction

A

Type 5 PDE inhibits - sildefanil

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20
Q

Give examples of how drugs might activate endogenous proteins

A

enzyme activators - GTNs activate guanylate cyclase

ion channel openers - K channel opener - minoxidil

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21
Q

what is compliance?

A

rigidity - when a vessel is compliant it is less stiff

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22
Q

what is afterload?

A

the stretch the l.ventricle undergoes to eject blood into the aorta

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23
Q

what is preload?

A

the end diastolic volume that stretches the l.ventricle prior to contraction

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24
Q

How might arterial compliance be affected by drugs?

A

anti-hypertensives - diuretics, ACE inhibitors, b-blockers
hypolipidemic agents - statins
anti-diabetic agents - thiazolidinediones
Treatment of congestive HF - ACE inhibitors, nitrates

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25
Q

What is the pressure wave?

A

the reflection of pressure back towards the heart at resistance points i.e. when the artery bifurcates

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26
Q

what happens to the pressure wave in patients with poor compliance?

A

it comes back quicker

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27
Q

what is the consequence of the faster returning pressure wave?

A

an increase in afterload -> hypertrophy -> heart attack and HF
lower diastole -> poor blood flow to coronary arteries -> ischemia
increased systolic pressue -> risk factor for stroke

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28
Q

how is contraction and maintenance of vascular tone mediated?

A

increases in IC Ca

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29
Q

Where might calcium be released from?

A

SR

plasma membrane channels VGCC or ROCC

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30
Q

What does calcium bind to influence contraction?

A

Ca - Calmodulin -> CaCaM + MLCK

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31
Q

What is the result of calcium-calmodulin binding MLCK?

A

phosphorylation of myosin

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32
Q

what is the result of myosin phosphorylation?

A

can bind actin to form actomyosin-P to cause contraction

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33
Q

How might increases in IC Ca cause a further increase in IC Ca?

A

activation of IP3R or RyRs

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34
Q

What hormones might act to regulate calcium increases?

A

AngII, NAdr, ET-1

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35
Q

How do calcium sparks act as a positive feedback?

A

increase smooth muscle contractility

36
Q

How do calcium sparks act as a negative feedback on contractility?

A

activation of Ca-sensitive K channels to cause hyperpolarisation causing limited constriction

37
Q

What underlies the process of calcium sensitisation?

A

phosphorylation of MLCP’tase inactivates the enzyme

agonist mediated activation of the rho/rho kinase pathway

38
Q

What underpins the process of vascular relaxation?

A

inhibition of Ca entry
hyperpolarisation of sm muscle membrane
increased cytoplasmic cAMP or cGMP
inhibition of Rho/Rho Kinase

39
Q

What do Ca Channel antogonists do?

A

block stimulated Ca influx

40
Q

What are some examples of Calcium channel blockers?

A

amlopidine, nifidepine

41
Q

What do Ca Channel blockers NOT do?

A

inhibit IC Ca release by specific agonists
reduce passive Ca entry
stimulate Ca Extrusion

42
Q

How is the SMC hyperpolarised?

A

closure of the VGCC
activation of Na-K-ATPase
Activation of K channels

43
Q

What inhibits the Na-K ATPase?

44
Q

What is the ratio of ions transported by the Na-K ATPase?

A

3 Na out for 2 K in

45
Q

What is the result of opening of K channels?

A

relaxation and hyperpolarisation

46
Q

What are the features of Kca channels?

A

present in SMC in most vascular beds
produce high amplitude K currents
expression is upregulated in pathological conditions i.e. arterial hypertension

47
Q

What are the features of Kv channels?

A

widely distributed and activated by membrane depolarisation
limited response to vasoconstrictors
altered expression may lead to pulmonary vasoconstriction and primary pulmonary hypertension

48
Q

What can cause pulmonary vasoconstriction and primary pulmonary hypertension?

A

altered expression of Kv channels

49
Q

What are the features of Kir channels?

A

voltage-dependent opening at more neg. potential

greatest expression in resistance arteries

50
Q

What are the features of Katp channels?

A

regulated by IC ATP

low activity in resting conditions

51
Q

What does cGMP activate?

52
Q

What does cAMP activate?

53
Q

How does PKG act?

A

to increase calcium uptake into SR and inhibit Ca influx

54
Q

How does PKA act?

A

to remove calcium to SR

55
Q

How do PKA and PKG act to prevent contraction?

A

dephosphorylate MLC

56
Q

What increases levels of cAMP and cGMP?

A

inhibitors of PDEs

57
Q

What is the dominant pathway of the ANS?

A

sympathetic nerves

58
Q

Where are the baroreceptors held?

A

carotid sinus and aortic arch

59
Q

What do the baroreceptors respond to?

A

temperature changes
outside communications
pressure changes

60
Q

What sort of innervation occurs at the sympathetic nerves?

A

Ach in preganglion -> NA at post ganglionic neuron

61
Q

Where are the ganglia located in the sympathetic NS?

A

in the spinal cord

62
Q

Where are the ganglia in the parasympathetic NS?

A

the target organ

63
Q

What are the NTs involved in the parasympathetic NS?

A

Ach and NO from cholinergic and then nitrergic neurons

64
Q

What does NA activate?

A

a/b adrenoceptors

65
Q

Where are a1 adrenoceptors located?

A

large arteries -> increases in Ca

66
Q

Where are a2 adrenoceptors located?

A

small arteries

67
Q

What is the effect of b-adrenoceptor activation

A

decreased vasoconstriction

68
Q

What are the types of endothelium?

A

continuous, discontinuous, fenestrated

69
Q

Which is the most common type of endothelium?

A

continuous

70
Q

What structures allow the transport of substances between cells?

A

plasmalemmal vesicles, channels, tight junctions

71
Q

Give examples of endothelium function

A 
barrier
permeability
vascular tone
inflammation
immunogenic processes
homeostasis
shear stress sensor
vascular growth
72
Q

How do bovine aortic endothelial cells adjust to blood flow?

A

within 6 hours they start to orientate in flow direction and within 24 hours totally orientated to cope with shear stress

73
Q

What is the response of damaged endothelium to Ach?

A

there is no response

74
Q

What are the endothelium derived vasodilators?

A

EDRF
prostacyclin
EDHF

75
Q

What are the endothelium derived vasoconstrictors?

A

ET-1

thromboxane

76
Q

What are the three isoforms of NOS?

A

nNOS - neuronal
iNOS - inflammation inducible
eNOS - endothelial

77
Q

What are the requirements of NO synthesis?

A

L-Arginine and O2

78
Q

What are the products of NO synthesis?

A

NO, L-citruline and NADP

79
Q

What are the common cofactors of NOS isoforms?

A

FAD, FMN and BH4

80
Q

Why is BH4 so important?

A

prevents ROS from damaging cells

important for redox uncoupling

81
Q

What inhibits BH4?

A

oxidative stress

82
Q

What occurs when BH4 is inhibited?

83
Q

which NOS are produced consituitively?

A

nNOS and eNOS

84
Q

Where is eNOS located?

A

membrane bound

85
Q

What is the effect of NO?

A

vasodilation

Cardiovascular Pharmacology (7 decks)

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