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sem 2 CVS > Cardiac Contraction > Flashcards

Cardiac Contraction Flashcards

1
Q

what is the duration of an action potential?

A

200-500 ms

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2
Q

what does opening the Na+ channels allow?

A

Allows Na+ to enter and depolarise

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3
Q

K+ channels opening allows what?

A

K+ efflux, so the membrane potential can be restored

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4
Q

what is the force of contraction proportional to?

A

The concentration of Ca2+

Higher increases in Ca2+ → increased force of contraction

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5
Q

During the depolarisation “plateau” phase what happens?

A

Ca2+ and cell shortening occur, CICR

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6
Q

muscle relaxation occurs when….?

A

when the cell is repolarised (when Ca2+ channels close and K+ channels open)

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7
Q

role of the Na+/K+ pump

A

pump 3 Na+ out, and pump 2 K+ in, maintain the “salty banana” analogy

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8
Q

what is CICR?

A

Calcium induced calcium release
Intracellular calcium levels increase from 0.1um to 10um, and this increase is detected by Ryanodine receptors on the SR, Ca2+ binds, which frees Ca2+ stored in the SR. .

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9
Q

what is the SR?

A

The sarcoplasmic reticulum, it’s a membrane bound structure within muscle cells similar to the ER in other cells. It stores Ca2+.

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10
Q

What are t-tubules?

A
  • Extensions/invaginations of the cell membrane (sarcolemma) that penetrate into the centre of cardiac muscle cells and get close to contractile fibres.
  • Inside t-tubules there are a lot of calcium channels.
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11
Q

what is the RyR?

A

the Ryanodine receptor, which is an intracellular Ca2+ channel

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12
Q

describe the whole process?

A

AP depolarises T-tubules and activates VGCC’s, causing an influx of Ca2+, which binds to RyR located on the SR (close association with t-tubules). Release of Ca2+ from the SR due to CICR, and the Ca2+ binds to troponin. Suppressive tropomyosin movves, exposing the active sites on actin. The myosin thick filament head binds to active sites, and the intrinsic ATPase activity releases energy, causing the filaments to slide.

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13
Q

A rise in [Ca2+] causes what?

A

Myosin-actin interactions

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14
Q

Myosin-actin binding sites are blocked by what?

A

troponin-tropomyosin complex

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15
Q

Troponin has 2 binding sites for what?

A

one for Ca2+, one for Tropomyosin

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16
Q

Binding of Ca2+to troponin causes what?

A

conformational changes of tropomyosin, exposing the binding site on actin

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17
Q

after the binding site on actin is exposed, what can the myosin head do?

A

the myosin head can bind to the actin, forming a cross-bridge

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18
Q

after the cross bridge there is a power stroke, what happens during this phase?

A

during the power stroke the myosin head bends, ADP and Pi released.

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19
Q

after the ADP and Pi are relased, what happens?

A

A new molecule of ATP attaches to the myosin head, causing it to detach from actin.

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20
Q

lastly after the new ATP binds what happens?

A

ATP hydrolysis to ADP and Pi, which returns the myosin to the energy-favourable cocked position ready to bind to actin

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21
Q

how many regulatory subunits is troponin made up of- name them and give their function:

A 
Troponin T (TnT)
-binds to tropomyosin
Troponin I (TnI)
-binds to actin filaments
Troponin C (TnC)
-binds to Ca2+
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22
Q

the binding of Ca2+ to TnC leads to what?

A

Conformation changes of tropomyosin and the exposure of actin binding sites for the myosin head to bind to.

23
Q

Take away the Ca2+ and what won’t happen?

A

muscle contraction

24
Q

When are TnI and TnT released into the bloodstream?

A

when cells in the heart die, for example in a heart attack (MI)

25
Q

why are TnI and TnT important?

A

They are important blood cell markers for cardiac cell death

26
Q

Decrease in [Ca2+] leads to what?

A

relaxation, myosin head ATPase activity releases energy, going from ATP to ADP

27
Q

explain fully what happens when there is a decrease in [Ca2+]:

A
  • There is AP repolarisation (K+ efflux) which repolarises T-tubules, VGCC close and VGKC open, K+ inside leaves, so relative charge inside is more negative inside
  • no Ca2+, no CICR
28
Q

what are the 2 ways to remove Ca2+ from a cell in order to reverse a contraction?

A
  1. Na+/Ca2+ exchanger in the cell membrane- 3Na+ in, 1 Ca2+ out
  2. Ca2+ uptake into the SR via SR Ca2+ ATPase, stored here until the next contraction. Uptake of Ca2+ into the mitochondria
29
Q

the prevention of the contraction mechanism means what?

A

the chambers are relaxed and can fill with blood

30
Q

what is the effect of NA on contraction, how does NA work?

A

-NA acts on β1-adrenoreceptors to increase contractility. The calcium response inside the heart is increased, which increases the force of contraction.

This occurs as:
-VGCC sensitivity is increased
OR
-efflux of Ca2+ from exchanger is reduced

31
Q

in the clinic why are drugs needed?

A

drugs are needed to increase contractility of the heart, mostly to correct acute or chronic heart failure

32
Q

what do these drugs do, and what is are they called?

A

they increase Ca2+ concentration, therefore increasing energy/strength of contraction

they are POSiTIVE INOTROPES

33
Q

these drugs can be split into 2 categories with separate methods of increasing Ca2+ concentration, what are they?

A
  1. Sympathetic mimetic-increase VGCC activity

2. Cardiac glycosides-reduce Ca2+ extrusion

34
Q

β1-adrenoreceptors induce what?

A

induce increased contractility

35
Q

where are β1-adrenoreceptors found?

A

β1-adrenoreceptors are found on the contractile cells of the heart, the atrial and the ventricular cells

36
Q

what happens when NA binds to the β1-adrenoreceptor?

A
  • Adenylate cyclase is stimulated to convert ATP to cAMP

- cAMP stimulus PKA, which phosphorylates VGCC, which are then activated and open to allow Ca2+ influx

37
Q

what is a positive ionotropic effect?

A

increased contractility of the heart

38
Q

what is a positive chronotropic effect?

A

increased heart rate

39
Q

what is a positive dromotropic effect?

A

increased conduction through AV node

40
Q

what is the lusitropic effect?

A

increased rate of relaxation, K+ channels and SR Ca2+ ATPase

41
Q

explain what increased PKA levels leads to:

A
  • Increased Ca2+ channel
  • Higher Ca2+ levels and greater contraction
  • Increased K+ channel opening, so faster depolarisation and shorter AP, meaning faster HR
  • Increased SR Ca2+ ATPase so uptake of Ca2+ into storage by SR allowing for faster relaxation
  • Overall stronger faster contractions but same diastolic time to allow for filling with blood and coronary perfusion
42
Q

what are cardiac glycosides?

A

they are called inotropes (positive inotropic action of the heart)

43
Q

how do cardiac glycosides work?

A

they inhibit the Na/K pump which maintains NA outside the cell. If there’s less Na+ outside, then there’s less Na+ that’s able to come in and expel calcium, which has the effect of not maintaining the relaxation period for long enough.

44
Q

give an example of a cardiac glycoside?

A

digoxin

45
Q

how does digoxin increase contractility?

A

reduce Ca2+ extrusion

46
Q

what is digoxin used for?

A

chronic heart failure

47
Q

what is digoxin not used so much now?

A

there are difficult side effects

48
Q

mechanism of action for digoxin:

A
  1. Digoxin inhibits Na+/K+ ATPase
  2. Build up of [Na+]
  3. Less Ca2+ extrusion by Na+/Ca2+ exchanger
  4. More Ca2+ uptake into stores and greater CICR
49
Q

name some other inotropic agents other than digoxin:

A
  • dobutamine and dopamine
  • glucagon
  • amrinone
50
Q

what are dobutamine and dopamine, and when are they used?

A

they are β1-adrenoreceptors stimulants

used in acute heart failure

51
Q

what does glucagon act as, what does it stimulate and when is it used?

A
  • acts as a GPCR
  • stimulates Gs pathway, increasing cAMP and PKA activity
  • used in patients with acute heart failure who are taking β-blockers
52
Q

what is amrinone and when is it used?

A
  • Amrinone is used a phosphodiesterase inhibitor
  • Phosphodiesterase (PDE) converts cAMP to AMP, ie. reducing cAMP and decreasing PKA activity, which reduces contractility
  • so, there is a build up of cAMP that activates PKA to phosphorylate VGCCs
53
Q

an inhibition of PDE leads to what?

A

PDE inhibition leads to a build up of cAMP that activates PKA to phosphorylate VGCC’s

54
Q

When is an increase in calcium ions used?

A

only used in severe cases, eg. those waiting for transplants

sem 2 CVS (17 decks)

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