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module 103 - theme 3 > molecular & ionic basis of cv control > Flashcards

molecular & ionic basis of cv control Flashcards

1
Q

what are the key characteristics of intrinsic regulation of cardiac muscle?

A
  • Frank-Starling relationship
  • increased contractility
  • longer and stronger
  • more crossbridges means more of everything
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2
Q

what are the key characteristics of extrinsic regulation of cardiac muscle?

A
  • sympathetic stimulation
  • faster and stronger
  • not longer durations
  • extant crossbridges work harder and faster
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3
Q

how does increased EVD (more stretch) lead to increased force of contraction?

A
  • increased overlap of thin and thick filaments
  • increased overlap leads to increased force generators
  • more of everything
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4
Q

how is heart rate controlled autonomically?

A
  • isolated or deneraved heart rate: approx 100 beats per min
  • the normal resting heart rate (about 60bpm) is due to tonic parasympathetic stimulation
  • heart rate is determined mostly by the slope of the pacemaker potential
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5
Q

what happens when noradrenaline increases funny current?

A
  • pacemaker channels
  • increases slope of pacemaker potential
  • via beta 1 receptor
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6
Q

what happens in nodal and ventricular areas with the sympathetic control of heart rate?

A
  • noadrenaline —> increased Ica: increased force of contraction
  • noadrenaline —> increased Ik: Ik = delayed rectifier, shortens AP duration, allows faster HR
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7
Q

what happens with the funny current if net current is inward?

A
  • technically it conducts both Na in and K out
  • non specific monovalent cation channel
  • the several potential of If is -10mv
  • it is not a sodium channel
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8
Q

what does sympathetic stimulation do to If?

A

increases If

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9
Q

what happens when HCN channel opens when membrane gets more negative?

A
  • controls slope of pacemaker potential

- Na/Ca exchange also helps with PP

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10
Q

what happens with vagal heart rate?

A
  • parasympathetic —> slower
  • acetylcholine —>increased K current Ik (Ach): hyperpolarises membrane, decreases slope pacemaker potential
  • Ach-activated K channel: G-protein (Gi) coupled, muscarinic
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11
Q

what are the types of K+ channels in cardiomyocytes?

A
  • delayed rectifiers
  • inward rectifiers
  • Ach-sensitive K channels Ik (Ach)
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12
Q

what happens during the neural action potential after hyperpolarisation?

A

this causes the voltage to go more negative than at rest:

  • after hyperpolarisation: at the end of an AP the voltage inside temporarily goes slightly more negative than at rest, followed by a return to the resting membrane potential
  • during the AHP the delayed rectifiers are still open, as the rest the delayed rectifiers are closed

the related rectifiers are open during the AHP because they are slow to close

  • during the AHP almost all the Na+ channels are inactivated
  • at rest there is a tiny amount of Na+ permeability

during the AHP: increased K+ permeability and decreased Na+ permeability —> membrane potential moves closer to Ek

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13
Q

why is the voltage during after-hyperpolarisation more negative than at rest?

A

both the delayed rectifiers & inwards rectifiers are open during early AHP

  • the inward rectifiers open when the membrane is more negative than -70mV
  • the delayed rectifiers are still open during the AHP because they are too slow to close
  • at rest the delayed rectifiers are closed

during AHP: increased K+ permeability and deceased Na+ permeability —> membrane potential moves very close to Ek

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14
Q

what is the refractory period?

A

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

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15
Q

what is an effective refractory period?

A
  • when it becomes nearly impossible to start a new action potential
  • in cardiomyocytes, lasts for duration of AP
  • protects the heart from unearned extra action potentials between SA node imitated heart beats: extra APs could start arrhythmias
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16
Q

what are T tubules?

A

invaginations of plasma membrane into monocyte

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17
Q

what are the purpose of T tubules?

A
  • so membrane currents can be near contractile machinery
  • contiguous with extracellular fluid
  • adjacent to SR
  • T tubule depolarises
  • terminal cisterna detects it
  • terminal cisterna sends it through ER
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18
Q

what is the terminal cisterna?

A

enlarged area of SR

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19
Q

what are the key characteristics of the terminal cisterna?

A
  • continuous with SR

- specialised for storing and releasing calcium

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20
Q

what is E-C 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

21
Q

what is excitation?

A

when a neuron stimulates the muscle cell

22
Q

how does voltage change lead to contraction?

A

diffusion of free calcium into the cytoplasm

23
Q

where does most the calcium come from during contraction?

A

sarcoplasmic reticulum

24
Q

what are some key characteristics of the sarcoplasmic reticulum?

A
  • where large concentrations of calcium is stored

- right next to the myocytes actin and myosin

25
Q

what happens to excitation-contraction coupling in skeletal muscle?

A
  • membrane depolarises
  • membrane calcium channels undergo a conformational change that opens them
  • calcium flows from SR to cytosol
26
Q

what are the key characteristics of ryanodine receptors (RyR)?

A
  • in SR membrane
  • channel that releases Ca2+
  • triggered by intracellular Ca2+ release
  • positive feedback loop
27
Q

where is SERCA found and what does it do?

A

found: SR membrane
function: pumps calcium back to SR

28
Q

what does sympathetic stimulation lead to in excitation-contraction coupling in cardiac myocytes?

A

increased Ec coupling which may cause calcium overload

29
Q

what happens with the process of calcium induced, calcium released?

A
  • this calcium is detected by calcium release channels on the SR
  • the calcium release channels (RyR) open, allowing calcium to flood form 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
30
Q

what are the issues with calcium overload?

A

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 and sympathetic drive
31
Q

where doe the 2 types of calcium channel blockers work?

A
  • on vessels: vasodilation, oppose hypertension

- on heart: anti anginal & antiarrhythmic agents

32
Q

what do the calcium channel blockers on the heart do?

A
  • reduce nodal rates and conduction through AV node

- makes heart failure worse

33
Q

what is Verapamil?

A
  • not a DHP
  • blocks calcium channels
  • used as antiarrhythmic
34
Q

what is Diltiazem?

A
  • not a DHP
  • blocks calcium channels
  • used as antianginal and antiarrhythmic
35
Q

what is digoxin?

A

positive inotropic agent

36
Q

what does digoxin do?

A
  • increases stroke volume

- increases contractility

37
Q

how does digoxin work?

A
  • it slightly inhibits Na/K pump in the membrane leading to increased calcium in the cytosol
  • stimulates vagus slowing heart rate and increasing AV delay
38
Q

what is digoxin used for?

A
  • atrial fibrillation

- can be used for heart failure but that is controversial

39
Q

how does myosin light chain kinase (MLCK) work?

A
  • vascular smooth muscle cell contraction initiated by MLCK
  • in smooth muscle, myosin must be phosphorylated to contract, increased of control by troponin and tropomyosin
  • MLCK phosphorylates myosin
  • MLCK is activated by calcium-calmodulin
  • relaxation occurs by dephosphorylating myosin: done by a phosphate activated by NO induced cascase
40
Q

how does nitric oxide (NO) work?

A
  • NO is made inside endothelial cells leading to vasodilation
  • relaxes vascular smooth muscle cells
  • as dissolved molecules, NO travels through VSMC membrane
  • inside VSMC, it activated an enzymatic cascade
  • cascade ends by dephosphorylation myosin which relaxes muscles
41
Q

which nitrates are used as vasodilators?

A
  • glyceryl trinitrate (GTN) = nitroglycerine

- prodrug: in body it degrades to produce NO

42
Q

how do nitrates work as vasodilators?

A
  • leads rapidly to vasodilation
  • continuous administration leads to tolerance
  • pulsed use works best
43
Q

how does bradykinin work as a peptide hormone?

A
  • loosens capillaries and blood vessels

- constricts bronchi and GI tract smooth muscle

44
Q

how does bradykinin dilate the arteriole?

A
  • endothelium dependent

- stimulates NO production in endothelium

45
Q

what are the 3 biomarkers in plasma?

A
  • troponin
  • creatine kinase (CK or CPK)
  • C reactive protein (CRP)
46
Q

what do you look for with troponin as a biomarker in plasma?

A
  • released from cardiomyocytes during necrosis
  • elevated during AMI, HF and many others
  • not elevated during unstable angina
47
Q

what do you look for with creatine kinase as a biomarker in plasma?

A

released from myocytes during necrosis

48
Q

what do you look for with C reactive protein as a biomarker in plasma?

A
  • increases in response to inflammation
  • acute phase protein
  • risk of CVD and future events

module 103 - theme 3 (17 decks)

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