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103 theme 3 > The molecular and ionic basis of cardiovascular control > Flashcards

The molecular and ionic basis of cardiovascular control Flashcards

1
Q

How is force of contraction of cardiac muscle regulated

A

Intrinsic regulation – starlings law, increased contractility, longer and stronger (more cross bridges, more of everything)
Extrinsic regulation – sympathetic stim, faster and stronger, not longer duration, extant cross bridges work harder and faster

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2
Q

how do sarcomeres link to starlings law

A

EDV inc – inc force of contraction

Increased overlap of thin and thick filaments (inc overlap – inc force generators so more of everything)

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3
Q

how is HR controlled autonomically

A

Isolated or denervated heart rate about 100 bpm
The normal resting HR is due to tonic ps stimulation (about 60 bpm)
HR determined mostly by slope of the pacemaker potential

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4
Q

how does sympathetic affect HR

A

NA – inc If (net inward current)
Pacemaker channels, inc slope of pacemaker potential, via B1 receptor
Also nodal and ventricular
NA inc Ca current (inc force of contraction)
NA inc K current
Delayed rectifier, shortens AP duration, allows faster HR

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5
Q

What is the funny current

A 
Net current is inward 
Technically conducts Na and K
Non specific monovalent cation channel
Reversal potential of -10mV
HCN channel opens when membrane gets more negative, controls slope of pacemaker potential (Na/Ca exchange)
Inc by sympathetic stimulation
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6
Q

what do a1 receptors do

A

PLC - PIP3 to IP3 and DAG - Ca2+ - vasoconstriction in most organs, sweat

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7
Q

what do B receptors do

A

Adenylyl-cyclase ATP to cAMP - inc contractility (B1), HR (If), skeletal muscle perfusion and bronchodilation(B2)

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8
Q

how does the vagus nerve affect HR

A

Parasympathetic – slower
Ach inc K current (hyperpolarises membrane, dec slope of pacemaker potential)
Ach activated K channel (G protein coupled, muscarinic)

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9
Q

How is HR slowed

A

Atropine blocks vagal slowing of HR (acts on M2 to stop ATP to cAMP IN SA and AV node)

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10
Q

how does the muscarinic receptor affect HR

A

Muscarinic Receptor slows HR

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11
Q

what K+ channels are found in cardiomyocytes

A

Delayed rectifiers
Inward rectifiers
Ach sensitive K channels

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12
Q

what happens during hyper polarisation

A

K+ permeability inc and Na+ dec, membrane potential closer to EKMore negative due to delayed rectifiers

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13
Q

Why voltage in after hyperpolarisation is more negative than at rest

A

Both delayed and inward rectifiers are open early during AHP
Inward open when membrane more negative than -70mV and delayed rectifiers slow to close
Leads to refractory period

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14
Q

What does the refractory period do

A

When it becomes nearly impossible to start a new action potential
In cardiomyocyte, lasts for duration of AP
Protects heart from unwanted extra Aps between SA node initiated heart beats - could start arrythmias

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15
Q

what are the t tubules and terminal cisternae

A

A system for strong and releasing calcium in response to Vm

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16
Q

what are t tubules

A

invaginations of plasma membrane into myocyte

17
Q

what do t tubules and terminal cisternae do

A

Triad – 1 t tubule surrounded by terminal cisternae
membrane currents can be near contractile machinery
Contiguous with extracellular fluid
Adjacent to SR
T tubule depolarises
Terminal cisterna detects it and sends throughout SR

18
Q

what are terminal cisternae

A

enlarged area of SR

Contiguous with SR, specialised for storing and releasing calcium

19
Q

what is excitation contraction coupling

A

The link between the depolarisation of the membrane (with tiny influx of Ca) and consequent huge inc in cytosolic Ca that leads to contraction
Excitation – when a neuron stimulates a muscle cell
Diffusion of free Ca into cytoplasm – voltage change – contraction

20
Q

E-C coupling in skeletal muscle

A

During contraction – most Ca comes from the sarcoplasmic reticulum (next to myocytes actin and myosin)
the membrane depolarises and calcium channels undergo a conformational change, calcium release channel in SR undergo a conformational change that opens them so Ca can flow in

21
Q

E-C coupling in cardiac myocytes

A 
Ryanodine receptor (RyR)
In SR membrane, channel that releases Ca, triggered by intracellular Ca inc, positive FB loop
SERCA in SR membrane, pumps Ca2+ back into SR (req ATP)
Sympathetic stimulation – inc EC coupling which may cause calcium overload
22
Q

how does calcium lead to calcium release

A

Initially Ca enters the cell from the outside
Calcium detected by calcium release channels in SP (intracellular), RyR open to allow Ca from SR to cytosol
Positive feedback loop
Close after a time delay
SERCA pumps Ca back into SR

23
Q

what results from excess calcium

A

Excessive intracellular Ca (also possibly xs Ca in SR)
Can cause risk of ectopic beats and arrythmias
Ca may spill out of SR into cytosol at inappropriate times in cardiac cycle, made worse by fast rates and sympathetic drives

24
Q

what are the different types of calcium channel blockers

A

On vessels – vasodilate, oppose hypertension (eg Amlodipine, a dihydropyridine)
On heart – anti-anginal and antiarrhythmic agents by reducing nodal rates and conduction through AV node but makes HF worse

25
Q

what does verapamil do

A

not a DHP, antiarrythmia
blocks heart more than vessel
slows nodal cells
protects V from rapd A rhythms (slow conduction to AV node)

26
Q

what does diltiazem do

A

not a DHP, antianginal and antiarrythmia
heart and vessel channels
slow nodal rate, vasodilator CAs, prevents angina (dec WL, inc perfusion)

27
Q

what is digoxin

A

Positive intropic agent – inc SV and contractility
Works by slightly inhibiting Na/K pump on membrane (inc Ca in cytosol) also stimulates Vagus (slows HR and inc AV delay)
Was used for HF (improves symptoms but not mortality, BB preferred)
Use now controversial, sometimes used for AF

28
Q

how is BP controlled locally

A

myogenic control
Endothelium detects stretch and plasma factors
Produced NO
Local hormones can affect the SM outside of endothelium
Endothelium controls vascular tone and clotting, responds to/makes Bradykinin and NO

29
Q

What does MLCK do

A

Vascular smooth muscle cell contraction initiated by MLCK
In SM, myosin must be phosphorylated to contract (instead of control by troponin and tropomyosin)
MLCK can phosphorylate myosin (at its light chain), activated by calcium-calmodulin
Relaxation occurs by dephosphorylating myosin, done by phosphatase activated by NO induced enzyme cascade

30
Q

how are VSMCs relaxed

A

dephosphorylating myosin by phosphatase activated by NO induced enzyme cascade
In peripheral skeletal muscles – B2 stimulation phosphorylates K channels leading to relaxation

31
Q

how are core organs and GI tract contracted

A

A1 stimulation phosphorylates MLCK – VSMC contraction

32
Q

How do nitrates act as

A

GTN degrades to produce NO
rapid vasodilation
continuous administration - tolerance

33
Q

what are bradykinins

A

Peptide hormone – loosens capillaries and BVs, constricts bronchi and GI tract smooth muscle

34
Q

what do bradykinins do

A

Vasodilator – endothelium dependant, stimulates NO production in endothelium
Increases capillary permeability eg inc saliva production

35
Q

what are the biomarkers in plasma

A

Troponin (Tn) – released from cardiomyocytes during necrosis
Elevated during AMI, HF and many others not elevated during unstable angina
Creatine Kinases (CK or CPK) – released from myocytes during necrosis
C reactive protein (CRP) – increases in response to inflammation
Acute phase protein

36
Q

how are bradykinins affected by ACE inhibitors

A

ACE inhibitors prevent degradation of bradykinin which causes dry cough associated with ACE inhibitors

103 theme 3 (20 decks)

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