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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

Intrinsic regulation

A

Frank-Starling relationship

Heart cells do it themseleves

Increased contractility

Longer and stronger

‘More crossbridges means more of everything’

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2
Q

Extrinsic regulation

A

Sympathetic stimulation

Dependent upon release of signal from another cell type

Faster and stronger

NOT longer duration

‘Extant crossbridges work harder and faster’

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3
Q

Sarcomeres and Frank-Starling law

A

Increased overlap leads to increased force generators

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4
Q

Heart rate: autonomic control

A

Isolated or denervated heart rate: 100bpm

Normal resting heart rate about 60bpm due to tonic parasympathetic stimulation

Heart rate determined mostly by slope of the pacemaker potential

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5
Q

Parasympathetic stimulation slows heart rate

A

Acetylcholine increases K conductance of SA node myocytes

Hyperpolarises cells and decreases the slope of the pacemaker potential

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6
Q

Sympathetic stimulation increases heart rate

A

Noradrenaline increases size of If which increases slope of pacemaker potential via beta 1 receptors

Noradrenaline increase ICa, speeds up upstroke of action potential and IK which shortens the action potential so allows faster HR

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7
Q

IK

A

delayed rectifier

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8
Q

Funny current If

A

Net current is inwards
- technically conducts Na in and K out

HCN channel opens when membrane gets more negative

  • controls slope of pacemaker potential
  • Na/Ca exchange also helps with PP
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9
Q

Alpha 1 adrenergic receptor

A

Gq

PIP3— IP3 + DAG (phospolipase C)

IP3 — Ca2+

Vasoconstriction in most organs
Sweat

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10
Q

Alpha 2 adrenergic receptor

A

Gi

Ca2+

ATP — cAMP (adenyl cyclase)

Less insulin
More glucagon

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11
Q

Beta receptor

A

Gs

ATP — cAMP (adenyl cylase)

Increased heart contractility
Increased heart rate
Increased skeletal muscle perfusion
Increased lypolysis in adipose

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12
Q

Heart rate: vagal

A

Parasympathetic –> slower

Acetylcholine –> increased K current

  • hyperpolarises membrane
  • decreases slope pacemaker potenetial

ACh- activated K channel

  • G-protein coupled
  • muscarinic
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13
Q

Atropine

A

Blocker of muscarinic receptor

Dilates pupils, increases heart rate and reduces salivation and other secretion

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14
Q

Beta 1

A

Beta 1 adrenergic receptor in heart cells

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15
Q

Beta 2

A

Beta 2 adrenergic receptors in vasculature in skeletal muscle

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16
Q

M2

A

Muscarinic receptors in heart

Blocked by atropine

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17
Q

Alpha 1

A

Adrenergic receptors in most vasculature

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18
Q

AII

A

Angiotensin 2 receptors in vasculature

Cause vasoconstriction

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19
Q

A1

A

Adenosine receptors

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20
Q

Neural action potential: after hyperpolarisation

A

Voltage below -60mV, inward rectifier K+ channels open again

Voltage more negative that at rest (delayed rectifiers are still open)

Delayed rectifiers are open during the AHP as slow to close

Increase in K+ permeability and decrease in Na+ permeability causes the membrane potential to move closer to EK

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21
Q

Effective refractory period

A

When it becomes nearly impossible to start a new action potential

In cardiomyocytes lasts for duration of AP

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

22
Q

T tubules

A

Invaginations of plasma membrane into myocyte

  • membrane current can be near contractile machinery
  • contiguous with extracellular fluid
  • adjacent to SR
  • T tubule depolarises ->
  • terminal cisterna detects it ->
  • terminal cisterna sends it throughout SR
23
Q

Terminal cisternae

A

Enlarged are of SR

  • contiguous with SR
  • specialised for storing and releasing calcium
24
Q

Triad

A

1 T tubule surrounded by terminal cisternae

25
Q

E-C coupling

A

The link between the depolarisation of the membrane and the consequent huge increase in cytosolic calcium that then leads to contraction

26
Q

Excitation

A

When a neurone stimulates a muscle cell

27
Q

Excitation contraction coupling in skeletal muscle

A

During contraction: most calcium comes from the sarcoplasmic reticulum

  • where calcium is stored
  • right next to myocyte’s actin and myosin

In skeletal muscle

  • membrane depolarises ->
  • membrane calcium channels undergo a conformational change ->
  • calcium release channels in SR undergo a conformational change that opens then ->
  • calcium flows from SR to cytosol
28
Q

Excitation contraction coupling in cardiac myocytes

A

Ryanodine receptor

  • in SR membrane
  • channel that releases Ca2+
  • triggered by intracellular Ca2+ increase
  • positive feeback loop

SERCA

  • in SR membrane
  • pumps Ca2+ back into SR

Pumping Ca back into SR requires ATP

Sympathetic stimulation leads to increased EC coupling

29
Q

SERCA

A

Smooth endoplasmic reticulum calcium ATPase

Calcium pump in the SR

Resequesters calcium and requires ATP to do so

30
Q

RyR

A

Ryanodine receptor

Clacium channel in the SR membrane of myocytes

31
Q

L-type calcium channel

A

Most common calcium selective channel

Voltage gated channel in plasma membrane

32
Q

Calcium induced calcium release

A

How EC coupling works in cardiomyocytes

  • calcium enters cell from outside
  • calcium detected by clacium release channels on the SR
  • calcium release channels (RyR) open, allow calcium to flood from SR to the cytosol
  • positive feedback loop
  • after a time delay, calcium release channels close
  • SERCA pumps the calcium back into the SR
33
Q

Calcium overload

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
34
Q

Calcium channel blockers

A

Different types

  • some act preferentially on vessels
  • others act pregerentially on the heart
35
Q

Calcium channel blockers on vessels

A

Vasodilate, oppose hypertension

  • amlodipine
36
Q

Calcium channel blockers on the heart

A

Anti-anginal and antiarrhythmic agents

  • reduce nodal rates and conduction through AV node
  • makes heart failure worse
37
Q

Amlodipine

A

Calcium channel blocker acts preferentially on vasculature

Used as anti-hypertensive

Dihydropyridine

38
Q

Non-DHP calcium channel blockers

A

Verpamil

Diltiazem

39
Q

Verapamil

A

Not a DHP

Blockes Ca2+

Used as antiarrhythmic

Blocks heart channels more than vessel channels

  • affects nodal cells
  • slows nodal rate
  • protects ventricles from rapid atrial rhythms
40
Q

Diltiazem

A

Not a DHP

Blocks Ca2+ channels

Used as antianginal and antiarrhythmic

Blocks heart and vessel channels

  • slows nodal rate
  • vasodilates coronary arteries
  • prevents angina by reducing workload while increasing perfusion
41
Q

Digoxin

A

Positive inotropic agent

  • increases stroke volume
  • increases contractility

Works by inhibiting Na/K pump on membrane leads to increase calcium in cytosol

Also stimulates vagus so slows heart rate and increases AV delay

Was used for heart failure, improves symptoms but not mortality

42
Q

Local control of blood pressure: myogenic control

A

Endothelium detects

  • stretch
  • plasma factors

Endothelium produces
- nitric oxide

43
Q

Myosin light chain kinase

A

VSMC contraction initiated by MLCK

In smooth muscle, myosin most be phosphorylated to contract
- instead of control by troponin and tropomyosin

MLCK phosphorylates myosin
MLCK is activated by calcium calmodulin

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

44
Q

Calmodulin

A

Regulatory protein in cytoplasm requires calcium binding to be active

45
Q

Nitric oxide

A

NO is made inside endothelial cells and causes vasodilation

Relaxes VSMC

As dissolved molecule, NO travels through VSMC membrane

Inside VSMC it activates and enzymatic cascade

Cascade ends by dephosphorylating myosin which relaxes muscle

46
Q

Nitrates and vasodilators

A

Glyceryl trinitrate- nitroglycerine

Prodrug: in body it degrafes to produce NO

Leads rapidly to vasodilation

Continuous administration -> tolerance

47
Q

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
- e.g. increases saliva production

ACE inhibitors prevent degradation of bradykinin

48
Q

Troponin

A

Released from cardiomyocytes during necrosis

Elevated during AMI, HF and many others

Not elevated during unstable angina

49
Q

Creatine kinase

A

Released from myocytes during necrosis

50
Q

C reactive protein

A

Increases in response to inflammation

Acute phase protein

Risk of cardiovascular disease and future events

103: Theme 3 (17 decks)

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