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40 > L14 - drug effects on smooth muscle > Flashcards

L14 - drug effects on smooth muscle Flashcards

1
Q

what organs contain smooth muscle

A

hollow ones

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2
Q

what regulates SM contraction

A

ANS
hormones
pacemaker cells (GI tract)

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3
Q

what type of drugs are used to affect smooth muscle of the cardiovascular system

A

vasodilators / constrictors

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4
Q

what type of drugs are used to affect smooth muscle of the genitourinary system

A 
anti muscarinics (M) 
B3 agonists
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5
Q

what type of drugs are used to affect smooth muscle respiratory system

A

B2 agonists (bronchodilation)

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6
Q

what are the two ways drugs can act on smooth muscle to produce effect

A
  1. act on receptors (as agonists/antagonists)

2. act on cell signal transduction (eg channel blockers)

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7
Q

effect of NA on blood vessels?

A

acts on a1 to cause constriction

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8
Q

effects of angiotensin 2 on blood vessels

A

(in blood) causes constriction

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9
Q

effects of adrenaline on blood vessels?

A

acts on a to constrict

acts on B2 to dilate

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10
Q

effects of increasing NO on blood vessels

A

vasodilation

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11
Q

describe the composition of actin and myosin in smooth muscle

A

actin is found within dense bodies
intermediate filaments link dense bodies
myosin found between dense bodies

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12
Q

describe process of SM contraction

A
  1. Ca2+ enters cytoplasm from SR and ECF
  2. Ca2+ binds to calmodulin and this complex activates MLCK
  3. MLCK phosphorylates myosin heads
  4. myosin forms cross bridges
  5. power stroke
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13
Q

what enzyme dephosphorylates myosin

A

myosin phosphatase

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14
Q

what is the effect of myosin phosphatase on SM contraction

A

causes myosin dephosphorylation - leads to relaxation of SM

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15
Q

what is Ca2+ sensitisation

A

the inhibition of myosin phosphatase (via rho kinase) causing smooth muscle contraction (independent of Ca2+ levels)

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16
Q

what is Ca2+ desensitisation

A

the activation of myosin phosphatase causing SM relaxation (independent of Ca2+ levels)

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17
Q

describe the mechanism of smooth muscle contraction via binding of noradrenaline / angiotensin 2

A
  1. bind to receptors (Gq coupled) which activates phospholipase C and rho kinase
  2. Phospholipase C breaks down PIP2 to DAG + IP3
    Rho kinase causes Ca2+ sensitisation)
  3. IP3 causes Ca2+ release from SR
    DAG opens Na+ and Ca2+ channels
  4. this causes depolarisation , which causes opening of voltage gated Ca2+ chnannels
  5. contraction
18
Q

what does rho kinase do

A

inhibits myosin phosphatase leading to Ca2+ sensitisation (SM contraction)

19
Q

what activates rho kinase?

A

the binding of agonist (NA/angiotensin 2) to G11 coupled receptor on smooth muscle

20
Q

what is EDRF?

A

endothelium derived relaxing factor - released by endothelium causing vasodilation

21
Q

describe process of vasodilation caused by NO (Ca2+ desensitisation)

A
  1. NO released from endothelium diffuses into SM
  2. stimulates guanylate cyclase which converts GTP to cGMP
  3. cGMP :
    • opens K+ channels (K+ out)
    • activates Ca2+ pumps (Ca2+ out)
  4. leads to Ca2+ desensitisation
  5. relaxation
22
Q

what are the effects of cGMP

A
  1. opens K+ channels (K+ out )
  2. activates Ca2+ pumps (Ca2+ out)

responsible for vasodilation

23
Q

what enzymes break down cGMP

A

phosphodiesterase’s

24
Q

main uses of vasodilators?

A

decrease b.p

treat angina

25
Q

what is the effect of Ca2+ channel blockers on contraction/dilation of SM

A

cause vasodilation

26
Q

what type of drugs cause vasodilation and can treat high b.p (and angina)

A 
Ca2+ channel blockers
ACE inhibitors
AT1 receptor antagonists 
a1 antagonists
minoxidil 
nicorandil 
organic nitrates
27
Q

what factors stimulate the renin-angiotensin-aldosterone system

A

decrease in

  • blood vol
  • blood Na+
  • blood pressure
28
Q

describe the R-A-A system

A
  1. renin released from JG cells of kidney cleaves angiotensinogen forming angiotensin 1
  2. Angiotensin converting enzyme (ACE) converts angiotensin 1 to angioensin 2
29
Q

what is ACE and what does it do

A

angiotensin converting enzyme

converts angiotensin 1 to angiotensin 2

30
Q

what receptor does angiotensin 2 act on

A

AT1 receptor

31
Q

what does activation of AT1 receptor by angiotensin 2 cause

A
  1. aldosterone release (increase blood vol,Na,pressure)
  2. ADH release (increase water reabsorption)
  3. vasoconstriction
32
Q

what does minoxidil do?

A

causes vasodilation by opening K+ channels leading to hyperpolarisation

33
Q

what does nicranodil do?

A

K+ channel agonist

stimulates guanylate cyclase

34
Q

give an example of a PDE5 inhibitor

A

sildenafil

35
Q

what does PDE5 do?

A

converts cGMP to GMP in blood vessels of penis (lower cGMP means vasoconstriction)

36
Q

what do a1 antagonists do to smooth muscle?

A

prevent binding of NA so the cellular mechanisms of contraction dont take place - vasodilation

37
Q

what does sildenafil do?

A

it is a PDE5 inhibitor which increases [cGMP] leading to vasodilation in blood vessels of penis treating erectile dysfunction

also dilates pulmonary arteries

38
Q

what do organic nitrates do?

A

breakdown to form NO
NO increases [cGMP]
vasodilation

39
Q

what drugs are used to treat an overactive bladder (contraction when it shouldnt)

A
  1. M2 and M3 antagonists
  2. B3 agonists
  3. botox
40
Q

what tupe of drugs can treat pulmonary hypertension

A
  1. stable PGI2 analogs (ileprost)
  2. PDE5 inhibitors (sildenafil)
  3. endothelin receptor antagonists (ambrisetan)

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