autonomic control of CVS Flashcards

1
Q

What does the ANS control in the CVS?

A

Heart rate Force of contraction Resistance of blood vessels

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2
Q

What does the ANS control in the CVS?

A
  • Heart rate
  • force of contraction
  • peripheral resistance of blood vessels
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3
Q

What is the parasympathetic input nerve to the heart?

What does it act on?

what GPCR is it?

what effect of inner action of this nerve does it have?

A
  • Vagus nerve - 10th cranial nerve
  • the SA node and AV node
  • M2 GPCR (Gi)
  • slows HR (negative chronotropic effect), decreases AV node conviction velocity to sloe HR further
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4
Q

What sympathetic input is there to the heart?

what does it act on?

what GPCR is used?

what is the effect of innervation?

A
  • Post ganglion is fibres from sympathies trunk
  • SA node, AV node and myocardium
  • B1 receptors (noradrenaline) (Gs)
  • positive chrontropic effect (inc HR), positive intropic effect (increase force of contraction)
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5
Q

Where does the parasympathiric and sympathetic control of the heart or originate from?

what are the affront inputs to this origination?

A
  • Cardiovascular control centre in the Medulla oblongata
  • baroreceptors (stretch receptors) in carotid sinus and aorta
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6
Q

What is teh sympathetic effect on the pacemaker potential in the SA node?

A

Shortens the time required to reach threshold

-noradrenaline acts on B1 receptors, B1 = Gs therefore when stimulated there is an increase in cAMP

more cAMP speeds up pacemaker potential

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7
Q

What is the parasympathetic effect on pacemaker potential?

A

Slows the time required to depolarise to threshold

it decreases the pacemaker slope

-ACh acts on M2 (Gi), therefore less cAMP is made mean inning less HCN channels are open

also Gi betagamma subunit acts on K+ channels and increases conductance

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8
Q

How does noradrenaline acting on B1 in the heart increases contraction?

A

B1= Gs = more cAMP

cAMP activates PKA

PKA phosphorylates L type Ca2+ channels in the sarcolemma and allows more Ca2+ in

it also increases Ca2+ uptake into the sarcoplasmic reticulum therefore has a bigger store of Ca2+ for consequent contractions

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9
Q

What type of innervation do all blood vessels receive?

what type do only some receive and give example?

A
  • Sympathetic
  • parasympathetic e.g. erectile vessels
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10
Q

What type of receptor do all vessels have for sympathetic innervation?

what type of receptor do only some have, give example?

A
  • All have A1 (A little hole)
  • some have B2 (skeletal muscle, liver, myocardium) - B = big hole
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11
Q

How does the sympathetic nervous system cause dilation and contraction of blood vessels?

A

There is a basal level of tone

less sympathetic input then this tone = dilation

more sympathetic input = constriction

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12
Q

What effect does adrenaline have on B2 receptors on blood vessels?

A

Adrenaline has a higher affinity for B2 than A1 in blood vessels

So at physiological conc B2 dilate the vessels

so dilation occurs

if adrenaline rises e.g. epipen - adrenaline will also bind to A1

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13
Q

How does binding to B2 cause vasodilation in blood vessels?

A

B2= Gs GPCR

this will produce cAMP and therefore activate PKA

PKA opens potasssium channels

PKA inhibits MLCK so cannot activate myosin light chain = no contraction = dilation

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14
Q

How does binding to A1 receptors in blood vessels cause vasoconstriction?

A

A1 = Gq GPCR

this produces IP3

IP3 causes more Ca2+ in the cell from SR = more contraction

Aldo DAG activate PKC

PKC inhibits MLCP therefore maintaining contraction = vasoconstriction

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15
Q

What is the role of local metabolites in blood vessels?

give example of local metabolites

A

They are important in vasodilation - more inmortant than B2

they ensure adequate perfusion of tissues

e.g. K+, H+, CO2

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16
Q

What are baroeceptors?

where are they located?

what are the afferent neurones?

talk me through the response to high BP

A
  • Stretch receptors that measure BP
  • aortic arch and carotid sinus
  • Aortic arch = vagus nerve, carotid sinus = glossopherngeal nerve, both go to CV control centre in medulla oblongata
  • the baroreceptors will stretch in high BP - this means more AP will be fired to the CV control centre - efferent neurones leaving the medulla oblongata will act on AV ans SA node to reduce HR and reduce BP in parasympathetic pathway - also vasodilation from less symp
17
Q

Can baroreceptors maintain BP over long term?

A

No - only good at short term control

With persistent high BP they reset at higher levels :(

18
Q

What are the 3 main classes of drugs acting on the ANS?

A
  1. Sympathomimics
  2. adrenoecptor antagonists
  3. cholongergics - M agonists and antagonists
19
Q

What do you use sympathomimetics for?

A
  • Adrenaline during cardiac arrest
  • Anaphylactic shock
  • B1 agonist on cardiogenic shock e.g. dobutamine
  • B2 for asthma e.g. salbutamol
20
Q

What are adrenoreceptor antagonists used for?

A
  • Antihypertensive agents acting on A1 e.g. prazosin
  • to slow HR and reduce contraction = B adrenoceptor e.g. propranolol (B1 bd @ so can cause bronchoconstriction:(), antenolol (just B1:)))))
21
Q

What are cholingergics used for?

A

Agonists e.g. pilocarpine to treat glaucoma by contracting m3 constrictor papillae muscle

antagonists e.g. atropine - increases HR, bronchial dilation and pupil dilation for examining eye

treats organophosphate poisoning