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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

(42 cards)

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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?

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A

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

18
Q

Describe what happens during after hyperpolarization (refractory period)

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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?

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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?

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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?

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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?

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A

A system for storing and releasing calcium in response to Vm

23
Q

What are T tubules?

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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?

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A

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

25
What are terminal cisterna and what is their function?
Enlarged area of SR Contiguous with SR Specialised for storing and releasing calcium
26
What is a triad?
1 T tubule surrounded by terminal cisternae
27
What is excitation- contraction coupling?
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
Describe the process of excitation contraction coupling in skeletal muscle?
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
Describe the process of excitation contraction coupling in the cardiac myocytes
``` 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
Describe calcium-induced calcium release
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
What is calcium overload and why is this a problem?
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
Describe verapamil
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
Describe Diltiazem
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
What is digoxin and how does it work?
``` 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
Describe myosin light chain kinase and its function
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
What is nitric oxide and where does it act? Describe how the cascade ends
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
What are Glyceryl Trinitrate (GTN)?
Nitroglycerine | Pro-drug in the body it degrades to produce NO and leads to rapid vasodilatation
38
Describe bradykinin
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
How do ACE inhibitors affect bradykinin?
ACE Inhibitors prevent degradation of bradykinin | Which causes dry cough associated with ACE inhibitors
40
Why is troponin used as a biomarker?
Released from cardiomyocytes during necrosis Elevated during AMI, HF and many others Not elevated during unstable angina
41
Why is creatine kinase used as a biomarker?
Released from myocytes during necrosis
42
Why is C reactive protein used as a biomarker?
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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