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Module 103: Theme 3: Physiology of the cardiovascular system. Principles of pathology, diagnosis and treatment of cardiovascular disease > The molecular and ionic basis of cardiovascular control > Flashcards

The molecular and ionic basis of cardiovascular control Flashcards

1
Q

Describe the intrinsic regulation of the force of contraction of cardiac muscle

A 
Frank-Starling relationship
  Increased contractility
  Increased preload
  Longer and stronger
  “More cross bridges means more of everything”
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2
Q

Describe the extrinsic regulation of the force of contraction of cardiac muscle

A

Sympathetic stimulation
Faster and stronger
NOT longer duration
“Extant cross bridges work harder and faster”

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3
Q

How does increased EDV (more stretch) cause an increase in the force of Contraction?

A

Increased Overlap of thin + thick filaments

Increased Overlap causes an increase in force generators

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4
Q

What is the isolated or denervated heart rate in beats per minute?

A

~100 beats per minute

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5
Q

What is the normal resting heart rate?

A

60 bpm

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6
Q

What is normal resting heart rate caused by?

A

Tonic (on all the time) parasympathetic (vagal) stimulation

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7
Q

What is heart rate mostly determined by?

A

The slope of the pacemaker potential

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8
Q

Which nervous supply is noradrenaline released in?

A

Sympathetic nervous system

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9
Q

What does noradrenaline do?

A

Noradrenaline Increases If (Net inward current)

  • increases slope of pacemaker potential
  • Via Beta 1 receptor

Also in nodal & ventricular:
Noradrenaline increases inflow of calcium which increases the force of contraction
Noradrenaline increases current of repolarizing potassium
-IK = delayed rectifier
-shortens AP duration
-Allows faster HR

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10
Q

Which direction is the net current in the funny current?

A

Inward

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11
Q

Which channel is involved in the funny current and when do they open?

A

HCN Channel opens when membrane gets more negative

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12
Q

What does an increase in sympathetic stimulation do to the funny current?

A

Increases

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13
Q

List the different types of adrenergic receptors

A

Alpha 1 - Gq, works using phospholipase C- responsible for vasoconstriction
Alpha 2- Gi, works using adenylyl cyklase- less insulin and more glucagon
Beta- Gs, stimulates adenylyl cyclase- heart contraction increases, increases heart rate, an increase in skeletal muscle perfusion and an increase in lipolysis in adipose tissue

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14
Q

Describe the parasympathetic supply to the heart

A

Acetylcholine leads to an increase in potassium current which hyperpolarizes the membrane and decreases the slope pacemaker potential

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15
Q

Describe the ACh activated potassium channel

A

Muscarinic

G protein coupled

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16
Q

What does atropine do?

A

Blocks the muscarinic receptor therefore blocks vagal slowing of heart rate and causes heart rate to increase. Useful in asystole

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17
Q

When do inward rectifiers open?

A

When the resting potential of the membrane decreases below -60mv

18
Q

Describe what happens during after hyperpolarization (refractory period)

A

During AHP: the ↑ K+ permeability and ↓ Na+ permeability. The membrane potential moves closer to EK

19
Q

Why are the delayed and inward rectifiers open during early after hyperpolarization?

A

The inward rectifiers open when the membrane is more negative than -70 mV
The delayed rectifiers are still open during the AHP b/c they are slow to close
At rest the delayed rectifiers are closed

20
Q

What is the effective refractory period and where does it occur?

A

When it becomes nearly impossible to start a new action potential
Occurs in cardiomyocytes

21
Q

What is the purpose of the effective refractory period?

A

Protects the heart from unwanted extra action potentials between SA node initiated heart beats
Extra APs could start arrhythmias

22
Q

What are T tubules and terminal cisternae used for?

A

A system for storing and releasing calcium in response to Vm

23
Q

What are T tubules?

A

Invaginations of plasma membrane into myocyte
So Membrane currents can be near contractile machinery
Contiguous with extracellular fluid
Adjacent to SR

24
Q

Describe what happens when T tubules are stimulated?

A

T tubule depolarises
Terminal Cisterna detects it
Terminal cisterna sends it throughout SR

25
Q

What are terminal cisterna and what is their function?

A

Enlarged area of SR
Contiguous with SR
Specialised for storing and releasing calcium

26
Q

What is a triad?

A

1 T tubule surrounded by terminal cisternae

27
Q

What is excitation- contraction coupling?

A

The link (molecular process) between the depolarisation of the membrane (with a tiny influx of calcium) and the consequent huge increase in cytosolic calcium that then leads to contraction

28
Q

Describe the process of excitation contraction coupling in skeletal muscle?

A

During Contraction: Most of the calcium comes from the sarcoplasmic reticulum
Where large concentrations of calcium are stored;
right next to the myocyte’s actin and myosin

In skeletal muscle
membrane depolarises
membrane calcium channels undergo a conformational change
calcium-release-channels in SR (RyR) undergo a conformational change that opens them
calcium flows from SR to cytosol

29
Q

Describe the process of excitation contraction coupling in the cardiac myocytes

A 
Ryanodine Receptor (RyR)
In SR membrane
Channel that releases Ca2+
Triggered by intracellular Ca2+ increase
Positive feedback loop

SERCA- The pump in SR membrane that pumps Ca2+ back into SR by pumping Ca back into SR requires ATP.
Sympathetic stimulation causing an increase in EC coupling which may cause calcium overload

30
Q

Describe calcium-induced calcium release

A

Initially Calcium enters the cell from the outside
This calcium is detected by calcium release channels on the SR (intracellular)
The calcium release channels (RyR) open, allowing calcium to flood from the SR to the cytosol
Positive feedback loop
After a time delay, the calcium release channels close
SERCA pumps the calcium back into the SR

31
Q

What is calcium overload and why is this a problem?

A

Excessive intracellular calcium
Also possibly excessive calcium in SR

Can cause risk of ectopic beats and arrhythmias
Calcium may “spill out” of SR into cytosol at inappropriate times in cardiac cycle
Made worse by: fast rates, sympathetic drive

32
Q

Describe verapamil

A

Not a DHP
Blocks Ca2+ channels
Used as antiarrhythmic

Blocks heart channels more than vessel channels
Affects nodal cells
Slows nodal rate
Protects ventricles from rapid atrial rhythms
Slows conduction through AV node

33
Q

Describe Diltiazem

A

Not a DHP
Blocks Ca2+ channels
Used as antianginal
Also antiarrhythmic

Blocks both heart and vessel channels (halfway)
Slows nodal rate
Vasodilates coronary arteries
Prevents angina by reducing workload while increasing perfusion

34
Q

What is digoxin and how does it work?

A 
Positive inotropic agent
Increases stroke volume
Increases contractility
Also called a “cardiac glycoside”
Works by (slightly) inhibiting Na/K pump on membrane
This leads to increase calcium in cytosol
Also stimulates vagus
Slows heart rate, increases AV delay

Was used for heart failure
Improves symptoms but not mortality
Beta blockers are preferred for CHF – decreases mortality
Digoxin is now sometimes used for atrial fibrillation

35
Q

Describe myosin light chain kinase and its function

A

Vascular Smooth Muscle Cell contraction initiated by MLCK
In smooth muscle, myosin must be phosphorylated to contract
Instead of control by troponin & tropomyosin
MLCK phosphorylates myosin (at its light chain)
MLCK is activated by Calcium-calmodulin

Relaxation occurs by dephosphorylating myosin
Done by a phosphatase activated by NO induced cascade

36
Q

What is nitric oxide and where does it act? Describe how the cascade ends

A

NO is made inside Endothelial cells —> vasodilatation
Relaxes Vascular Smooth Muscle Cells (VSMC)
As dissolved molecule, NO travels through VSMC membrane
Inside VSMC, it activates an enzymatic cascade
Cascade ends by dephosphorylating myosin
Which relaxes muscle

37
Q

What are Glyceryl Trinitrate (GTN)?

A

Nitroglycerine

Pro-drug in the body it degrades to produce NO and leads to rapid vasodilatation

38
Q

Describe bradykinin

A

Peptide hormone
“Loosens” capillaries and blood vessels
Constricts bronchi and GI tract smooth muscle

Vasodilator
Endothelium-dependent
Stimulates NO production in endothelium

Increases capillary permeability

39
Q

How do ACE inhibitors affect bradykinin?

A

ACE Inhibitors prevent degradation of bradykinin

Which causes dry cough associated with ACE inhibitors

40
Q

Why is troponin used as a biomarker?

A

Released from cardiomyocytes during necrosis
Elevated during AMI, HF and many others
Not elevated during unstable angina

41
Q

Why is creatine kinase used as a biomarker?

A

Released from myocytes during necrosis

42
Q

Why is C reactive protein used as a biomarker?

A

Increases in response to inflammation
Acute phase protein
Risk of cardiovascular disease & future events

Module 103: Theme 3: Physiology of the cardiovascular system. Principles of pathology, diagnosis and treatment of cardiovascular disease (19 decks)

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