Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHAR2002 > Smooth Muscle > Flashcards

Smooth Muscle Flashcards

1
Q

Mech of smooth muscle contraction

A
  1. Increase I.C. Ca2+
  2. Ca 2+ binds calmodium
  3. Ca-calmodium activates MLCK
  4. Phosphorylates MLC’s in presence of ATP
    - > 20-kd reg, subunits in myosin head
  5. Cross-bridge formation -> s.m. contracts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Ca2+ movement in blood vessels

A
  1. Ca2+ enters cell from external environment
  2. Ca2+ released by I.C. storage sites (SR) -> ATP-dep ca2+ pump
  3. Removal -> ATP- dep. Ca2+ pump/ Na+/ Ca2+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Arterioles

A

Small, thick-walled vessels -> vascular resistance ->

“circulatory stopcocks”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Oedema is caused from

A

Increased capillary hydrostatic pressure / increased capillary permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Venules/ veins

A

Highly distensible + large fraction blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Systematic venules/veins ->

A

Volume reservoir approx. 5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

VSM contraction

A
  1. Mech -> myogenic response -> passive
  2. Elec. -> opening L-type Ca channels
  3. Chem.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does NA bind to VSM?

A

From sympathetic nerves via a1-adrenoreceptors coupled via Gq to PLC + InsP3 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Co-transmitters for NA

A
  • ATP - can cause contraction via activation of non-selective cation channel e.g. P2X
  • Gq coupled to PLC e.g. P2Y
  • NPY mech of action not clear but potentiate action ofNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alpha 1- adrenoreceptor antagonists act as

A

Vasodilators e.g. prazosin, indoramine -> cause vasodilation + fall in bp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Amphetamine, tyramine and ephendrine mech. of action

A

Indirect acting vasoconstrictors that cause NA release from nerve terminals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cocaine effect

A

Sympathomimetic effect -> Blocks uptake of NA into nerve terminals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is Angiotensin II produced?

A

ATI -> ATII by ACE in vascular endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Example of ACE inhibitor

A

Catopril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does AII lead to VSM contraction

A

acts via AI receptors coupled via Gq to PLC + Insp3 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Endothelin (ETA and ETB2) characteristics

A

21 aa peptides, 3 isoforms

17
Q

How does ET1 lead to VSM contraction

A

ET1 acts via ETA and ETB2 receptors coupled to Gq

18
Q

Endothelin antagonists

A

BQ-123, BMS 182874

19
Q

Vasporessin is a

A

Posterior pituitary hormone with major actions on kidney

20
Q

Vascular actions of VP

A

Via V1 receptors to elicit VSM contraction + constriction of GI and uterine SM

21
Q

What is the name of a VP analog and how is it used?

A

Felypressin -> vasoconstrictor with LA’s

22
Q

How does ergotamine work to reduce migraine?

A

Migraine = dilation of cerebral blood vessels

-> ergotamine -> marked vasoconstriction

23
Q

How does sumatriptan act to reduce migraine?

A

5-HT1D like receptor agonist -> constricts intracranial vascular smooth muscle - possibly trigeminal muscles

24
Q

Mechanism of VSM relaxation

A
  1. cAMP stimulation of PKA -> phosphorylates and opens KATP channels.
  2. hyperpolarization of smooth muscle cells
    and closing of voltage-gated Ca2+ channels.
  3. decreases intracellular [Ca2+] and so MLC phosphorylation, thereby
  4. decreasing the interactions between actin and myosin. 5. drugs which increase cAMP (e.g., 2-adrenoceptor agonists, phosphodiesterase inhibitors) cause vasodilation.
25
Q

How does NO regulate VSM tone?

A

Through cGMP :
cGMP can activate a cGMP-dependent
protein kinase, inhibit calcium entry into the VSM, activate K+ channels, and decrease IP3.

26
Q

NO drugs:

A
  1. Nitrovasodilators
  2. NO -> respiratory disease syndrome
  3. Drugs that act via receptors on endothelium to stimulate NO synthase
  4. NO inhibitor for septic shock
27
Q

How does viagra work?

A

Pelvic stimulation -> NO release -> relax sm of corpus cavernosum -> NO metabolised by PDE-5
Sildenafril (viagra) inhibits PDE-5

28
Q

Nifedipine

A

Calcium antagonist -> block calcium channel -> fall bp + reflex tachycardia

29
Q

Ipratropium bromide

A

Muscarinic receptor antagonist -> used as an anti-asthmatic drug + given by aerosol inhalation

  • quaternary compound so low lipid solubility
  • can’t cross BBB
30
Q

Theoprylline (aminophylline)

A

Methyl xanthine bronchodilator q

31
Q

Oxytocin

A

PPH hormone

  • slow IV infusion to induce labour -> regular contractions
  • higher doses: reduce postpartum haemorrhage
32
Q

Ergometrine use in uterine SM

A

Evokes contraction of sm used with oxytocin to contract uterus

33
Q

Therapeutic abortion drugs

A

Prostaglandins E2 and F2a -> marked rythmical contractions

34
Q

Salbutamol

A
  • SM relaxation -> beta 2 - adrenoreceptor antagonist

- premature labour -> relax uterine muscle

PHAR2002 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions