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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

(50 cards)

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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

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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

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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

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A

Enlarged are of SR

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

Triad

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A

1 T tubule surrounded by terminal cisternae

25
E-C coupling
The link between the depolarisation of the membrane and the consequent huge increase in cytosolic calcium that then leads to contraction
26
Excitation
When a neurone stimulates a muscle cell
27
Excitation contraction coupling in skeletal muscle
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
Excitation contraction coupling in cardiac myocytes
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
SERCA
Smooth endoplasmic reticulum calcium ATPase Calcium pump in the SR Resequesters calcium and requires ATP to do so
30
RyR
Ryanodine receptor Clacium channel in the SR membrane of myocytes
31
L-type calcium channel
Most common calcium selective channel Voltage gated channel in plasma membrane
32
Calcium induced calcium release
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
Calcium overload
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
Calcium channel blockers
Different types - some act preferentially on vessels - others act pregerentially on the heart
35
Calcium channel blockers on vessels
Vasodilate, oppose hypertension - amlodipine
36
Calcium channel blockers on the heart
Anti-anginal and antiarrhythmic agents - reduce nodal rates and conduction through AV node - makes heart failure worse
37
Amlodipine
Calcium channel blocker acts preferentially on vasculature Used as anti-hypertensive Dihydropyridine
38
Non-DHP calcium channel blockers
Verpamil Diltiazem
39
Verapamil
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
Diltiazem
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
Digoxin
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
Local control of blood pressure: myogenic control
Endothelium detects - stretch - plasma factors Endothelium produces - nitric oxide
43
Myosin light chain kinase
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
Calmodulin
Regulatory protein in cytoplasm requires calcium binding to be active
45
Nitric oxide
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
Nitrates and vasodilators
Glyceryl trinitrate- nitroglycerine Prodrug: in body it degrafes to produce NO Leads rapidly to vasodilation Continuous administration -> tolerance
47
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 - e.g. increases saliva production ACE inhibitors prevent degradation of bradykinin
48
Troponin
Released from cardiomyocytes during necrosis Elevated during AMI, HF and many others Not elevated during unstable angina
49
Creatine kinase
Released from myocytes during necrosis
50
C reactive protein
Increases in response to inflammation Acute phase protein Risk of cardiovascular disease and future events

103: Theme 3 (17 decks)

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