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T2: Theme 3: CVS > Lecture 18: Ionic basis of cardiovascular control > Flashcards

Lecture 18: Ionic basis of cardiovascular control Flashcards

1
Q

What comprises the intrinsic regulation of the cardiac muscle contraction?

A

Frank-Starling relationship

Increased contractility

Longer and stronger

“More crossbridges means more of everything”

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2
Q

What comprises the extrinsic regulation of the cardiac muscle contraction?

A

Sympathetic stimulation

Faster and stronger

NOT longer duration

“Extant crossbridges work harder and faster”

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3
Q

What is the natural rate of an isolated or denervated heart?

A

100bpm

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4
Q

What determines heart rate?

A

Slope of the pacemaker potential

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5
Q

What is the effect of noradrenaline (sympathetic) on the If channel?

A

Increases activity - net inward current

Increases slope of the pacemaker potential (increases rate)

Acts on Beta1 receptors

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6
Q

What is the effect of noradrenaline (sympathetic) on the Ca channels?

A

Increases force of contraction

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7
Q

What is the effect of noradrenaline (sympathetic) on the delayed rectifier K channels?

A

Shortens AP duration

Faster heart rate

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8
Q

What is the HCN channel?

A

Non-specific monovalent cation channel

Opens when the membrane gets more negative

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9
Q

What is the effect of sympathetic activity of If?

A

Increases If

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10
Q

What is the reverse potential of If?

A

-10mV

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11
Q

What pathway is activated by Gq?

A

PLC - IP3 - DAG
Ca

Vasoconstriction in most organs

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12
Q

What pathway is activated by Gs?

A

Adenylate cyclase - cAMP

Increase contractility, HR, perfusion of skeletal muscles, lipolysis in adipose tissue

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13
Q

What pathway is deactivated by Gi?

A

Adenylate cyclase - cAMP

Less insulin, more glucagon

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14
Q

What is the effect of acetylcholine on heart rate?

A

Vagal - parasympathetic

Increases K current so hyper polarises the membrane

Decreases the slope of the pacemaker potential

Slows HR

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15
Q

What is atropine?

A

Blocker of muscarinic receptor - blocks vagal slowing of HR

So increases HR

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16
Q

When do the inward rectifier K+ channels open?

A

When the voltage goes below -60mV

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17
Q

During the AHP which channels are open?

A

Delayed rectifiers and inward rectifiers are open

Almost all Na channels are inactivated

18
Q

What is the refractory period?

A

When there is so much positive current leaving the cell, it is impossible to depolarise it again

19
Q

At what stage are the delayed rectifier channels closed?

A

When the membrane is at rest

20
Q

What is the effective refractory period (ERF)?

A

When it becomes nearly impossible to start a new action potential

In cardiomyocyte, lasts for duration of AP

Protects the heart from unwanted extra action potentials between SA node initiated heart beats

21
Q

What are T-tubules?

A

Invaginations of plasma membrane into myocyte

T tubule depolarises –> terminal Cisterna detects it –> terminal cisterna sends it throughout SR

22
Q

What is the terminal cisternae?

A

Enlarged area of SR

Specialised for storing and releasing calcium

23
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 cytosolic calcium that then leads to contraction

24
Q

What is the primary control of cardiac muscle contraction?

A

Diffusion of free calcium into the cytoplasm

25
Q

Where are large concentrations of calcium stored in the skeletal muscle?

A

Sarcoplasmic reticulum

26
Q

What is the name of the receptor on the terminal cisterna that allows the release of large amounts of calcium?

A

Ryanodine receptors

27
Q

What is the name of the receptor in the cell membrane that allows a small influx of calcium into the cell to activate the RyR?

A

DHPR

28
Q

What is the role of SERCA?

A

In the SR membrane - pumps calcium back into the SR

Requires ATP

29
Q

What is the effect of sympathetic stimulation of the EC coupling?

A

Increases EC coupling

30
Q

What may be caused by calcium overload?

A

Risk of ectopic beats and arrhythmia

31
Q

What is the effect of a DHP calcium channel blocker.

A

Vasodilates - opposes hypertension

Amlodipine

32
Q

What is the effect of non-DHP calcium channel blockers?

A

Anti-anginal and anti-arrhythmic

BUT makes heart failure worse

Verapamil - anti arrhythmic (blocks heart vessels)

Diltazem - anti-anginal and anti arrhythmic (blocks hear and vessel channels)

33
Q

What is digoxin?

A

Positive inotropic agent - increases stroke volume and contractility

Works by inhibiting Na/K pump - causes increased Ca in the cytosol

Also stimulates vagus - slows HR

Used for AF

34
Q

What is the effect of beta2 stimulation on VSMCs in peripheral skeletal muscles?

A

Cause VSMC relaxation

B2 - cAMP - PKA - p-MLCK (inactive when phosphorylated) - can’t phosphorylate or activate myosin

35
Q

What is the effect of alpha1 stimulation on VSMCs in core organs and GI tract?

A

Smooth muscle contraction

A1 - PLC - IP3 - Ca - CaM - MLCK (activate when bound to Ca-CaM) - p-myosin

36
Q

What is bradykinin?

A

Peptide hormone that loosens capillaries and blood vessels

Vasodilator - stimulates NO production in endothelium

Increases capillary permeability - increases saliva production

37
Q

What is the effect of ACE inhibitors on bradykinin?

A

ACE inhibitors prevent degradation of bradykinin - causes dry cough

38
Q

When is creatinine kinase released from myocytes?

A

During necrosis

39
Q

When is CRP released?

A

Increased in response to inflammation

40
Q

When is troponin released from cardiomyocytes?

A

During necrosis - elevated during AMI but not during unstable angina

T2: Theme 3: CVS (18 decks)

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