Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVS > electrical and molecular mechanisms > Flashcards

electrical and molecular mechanisms Flashcards

1
Q

K+ permeability sets resting membrane potential (RMP)

A
  • cardiac myocytes permeable to K+ ions at rest
    • move out of cell down conc. gradient
  • small outward movements of ions makes inside negative relative to outside- as charge builds up electrical gradient established
  • RMP doesn’t exactly equal EK (-95mV) as other ions make RMP = between -90 to -85 mV
  • AP triggers increase in cytosolic Ca2+ - from stores + exctracellular influx - rise in CA2+ needed for actin-myosin interactions leading to contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

cardiac (ventricular) action potential

N.B. there are many type of K+ channels in cardiac myocytes and each behaves and contributes differently to the electrical properties of the cell

A
  • RMP due to background K+ channels
  • Upstroke due to opening of voltage-gated Na+ channel - influx of Na+
  • Initial repolarisation due to transient outward K+ channels (V-gated ito)
  • Plateau due to opening of voltage-gated Ca2+ channels (L-type) - influx of Ca2+ - balanced by K+ efflux (iKV)
  • Repolarisation due to efflux of K+ through voltage-gated K+ channels (iKV iKR) and others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

the SAN action potential

A
  1. initial slope towards threshold potential (50mV) caused by funny current - HCN channels bring NA into cells - the mkre negative the more it activates
  2. depolarisation (upstroke) caused by opening of voltage gated Ca ion channels - Ca ions move in
  3. Repolarisation caused by opening of voltage-gated K+ channels as potassium ions move out of cell returning cell to resting membrane potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

SAN is the pacemaker of the heart

A

SAN action potential has natural automaticity. funny current due to unstable membrane potential of pacemaker and its slow depolarisation to threshold

  • APs throughout heart have varying waveforms
  • SAN fastest to depolarise – sets rhythm- is the pacemaker – other parts of conducting system also have automaticity but are slower
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

AP variation issues

A
  • If action potentials fire too slowly → bradycardia
  • If action potentials fail → asystole - heart ceases to beat
  • If action potentials fire too quickly → tachycardia
  • If electrical activity becomes random → fibrillation (rapid, irregular + unsnchronised contraction of muscle fibres)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hyperkalaemia 1

A
  • normal [K+] = 3.5 to 5.5 mmol/L,
  • hyperkalaemia when K+> 5.5
  • If increase in the K+ plasma concentration, EK becomes more positive + so RMP depolarises a little bit
    • leading to inactivation of some of the voltage-gated Na+ channels (which slows upstroke)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hyperkalaemia 2

A
  • Hyperkalemia can cause the heart to go into Asystole
  • Initially might be increase in excitability of the heart
  • mild = 5.5-5.9 mmol/l
  • moderate = 6-6.4 mmol/L
  • severe> 6.5mmol/L

treatment

  • If heart has already stopped, the above won’t work
  • Insulin + glucose
  • Calcium gluconate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hypokalaemia

A

K+ less than 3.5mmol/L

  • Lengthened action potential and delayed repolarisation
  • Longer AP can lead to early after depolarisations (EAD)
    • This can lead to oscillations in membrane potential
    • Can result in ventricular fibrillation = no cardiac output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

excitation - contraction coupling

A
  • depolarisation of membrane of myocytes opens L type calcium channels in T- tubule system
  • entry of Ca2+ ions causes CICR(calcium induced calcium release) channels to release more Ca2+ from sarcoplasmic reticulum
  • 25% enters across sarcolemma, 75% released from SR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

regulation of cardiac myocyte contraction and relaxation

A
  • Ca2+ binds to troponin C - conformational change - moves tropomyosin to reveal binding site for myosin

relaxation- must return Ca2+ to resting levels

  • most pumped back into SR by SERCA (raised Ca2+ stimulates the pumps)
  • some exits across cell membrane
    • sarcolemmal Ca2+ATPase
    • Na+/Ca2+ exchanger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

vascular smooth muscle contraction 1

A
  • Ca2+ enters through VGCCs/IP3 binds to IP3 receptors on SR causing release of Ca2+
  • Ca2+ binds to calmodulin (CaM)
  • activates myosin light chain kinase (MLCK)
  • MLCK phosphorylates myosin light chain enabling actin- myosin interaction → contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

vascular smooth muscle relaxation

A

relaxation as Ca2+ levels decline

  • myosin light chain phosphatase (MLCP) dephosphorlates myosin light chain
  • note: MLCK can itself be phosphorylated
  • Phosphorylation of MLCK by PKA inhibits action of MLCK – therefore inhibiting contraction as actin-myosin interactions not enabled
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

to conclude

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

the Autonomic Nervous System (ANS)

A

ANS important in regulation of many physiological functions

  • heart rate, bp, etc. (homeostasis)
  • exerts control of smooth muscle (vascular + visceral), exocrine secretion, heart chronotropy & inotropy

Divided into sympathetic and parasympathetic nervous systems, these divisions are based on anatomical grounds

  • GI has a separate nervous system but is supplied by Symp. and Parasymp. Fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

functions of ANS

A
  • Regulation of physiological functions
  • Symp. & Parasymp. Tend to have opposite effects where they both innervate the same tissue
  • Stress increases sympathetic activity
  • Parasympathetic system more dominant under basal conditions
  • Symp. + Parasymp. Systems work together for balance

Sympathetic drive to different tissues is independently regulated but there can be a more coordinated sympathetic response i.e. fight or flight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

control of CVS by ANS

A

controls heart rate, force of contraction of heart, TPR of blood vessels, + amount of vasocnstriction

ANS does not initiate electrical activity on the heart

  • denervated heart still beats but at faster rate (around 100bpm)
  • at rest heart is normally under vagal influence
17
Q

parasympathetic input to heart

A

Vagus nerve = 10th cranial nerve = parasympathetic innervation of heart

  • Synapse with postganglionic cells on epicardial surface or with in walls of heart at SA and AV node
  • Post ganglionic cells release ACh- Acts on M2-receptors
    • Decrease heart rate (negative chronotropic effect)
    • Decrease AV node conduction velocity
18
Q

Sympathetic input to the heart

A
  • postganglionic fibres from sympathetic trunk
  • innervate SAN, AVN, myocardium – release noradrenaline
  • mainly acts on β1 adrenoceptors
    • increases heart rate ( +ve chronotropic effect)
    • increases force of contraction (+ve inotropic effect)
  • β2 & β3 adrenoceptors are also present in heart, main effect is mediated by β1 adrenoceptors
19
Q

SAN

A
  • Initial slope to threshold – If (funny current)
  • Activated at membrane potentials that are more negative than – 50mV
  • The more negative, the more it activates
  • HCN channels – Hyperpolarisation-activated, Cyclic Nucleotide-gated channels
    – Allow influx of Na+ ions which depolarises the cells
20
Q

Noradrenaline (NA) increases force of contraction

A
  • NA ating on ß1 receptors in myocardium causes an increase in Camp → activartes PKA
    • Phosphorylation of Ca2+ channels increase Ca2+ during plateau of the AP
    • Increased uptake of Ca2+ in sarcoplasmic reticulum
    • Increased sensitivity of contractile machinery to Ca2+

→ all lead to increased force of contraction

21
Q

ANS effect on vasculature

A

Most vessel receive sympathetic innervation – some exceptions – e.g. some specialised tissue e.g. erectile tissue has parasympathetic innervation

Most arteries and veins have a1- adrenoreceptors – coronary and skeletal muscle vasculature also have β2- receptors

  • Circulating adrenaline has higher affinity for β2 adrenoreceptors than α1 receptors
  • At physiological concentration circulating adrenaline will preferentially bind to β2 adrenoreceptors
  • At higher conc. → also activates α1 receptors
22
Q

Effects of b2 and a1 adrenoreceptors on vascular smooth muscle

A

activating B2 adrenoreceptors causes vasodilation

  • increases cAMP → activates PKA →opens potassium channels + inhibits MLCK →relaxation of smooth muscle

Activating α1 adrenoreceptors causes vasoconstriction

  • Stimulates IP3 production
  • increase in [Ca2+] in from stores and via influx of extracellular Ca2+
  • contraction of smooth muscle
23
Q

local metabolites

A
  • Active tissue produces more metabolites e.g. adenosine, K+, H+, increase PCO2. Local increases in metabolites have a strong vasodilator effect
  • Metabolites are more important for ensuring adequate perfusion of skeletal and coronary muscle than activation of β2-receptors
24
Q

baroreceptors

A
  • Baroreceptors (high pressure side of system)
  • Atrial receptors (low pressure side of system)
  • Changes in state CVS communicated back to brain via afferent nerves
    • brain then alters the activity of efferent nerves
  • Baroreceptors are found in the carotid sinus and the aortic arch.
25
Q

baroreceptor reflex

A
  • The baroreceptor reflex is important for maintaining blood pressure over short term.
  • It compensates for moment to moment changes in arterial BP HOWEVER…. Baroreceptors can re-set to higher levels with persistent increases in blood pressure (hypertension)
26
Q

Sympathomimetics – mimic sympathetic NS

α-adrenoceptor agonists & β-adrenoceptor agonists

A

cardiovascular uses

  • administration of adrenaline to restore function in cardiac arrest
  • β1 agonist – dobutamine may be given in cardiogenic shock (pump failure)
  • adrenaline administered for anaphylactic
  • other uses – β2 agonists – salbutamol for treatment for treatment of asthma
27
Q

adrenoreceptor antagonists

α-adrenoceptors

A

α-adrenoceptors:

  • α1-antagonists – e.g. prazosin
  • anti-hypertensive agent – but only to be used with resistant hypertension - inhibits NA action on vascular smooth muscle α1 receptors → vasodilation
28
Q

adrenoreceptor antagonists - ß adrenoceptors

A
  • propranolol – non-selective β1 /β2 antagonist
    • slows heart rate and reduces force of contraction (β1)
    • also acts on bronchial smooth muscle (β2) -> bronchoconstriction
  • Atenolol – selective β1 (cardio-selective) – less risk of bronchoconstriction
29
Q

Cholinergics

A

Muscarinic agonists

  • e.g. pilocarpine – used in treatment of glaucoma
    • activates constrictor pupillae muscle

Muscarinic antagonists

  • e.g. atropine or tropicamide
    • increases heart rate, bronchial dilation
    • used to dilate pupils for examination of the eye

CVS (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions