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Cardiovascular System > Autonomic Control > Flashcards

Autonomic Control Flashcards

1
Q

What activity is up is cardiovascular disease

A

Cardiac and renal sympathetic nerve activity. Whereas skin SNA is more for thermocontrol, and doesn’t change in cardiac disease.
Sympathetic is not just fight or flight, much more complicated then that

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2
Q

Somatic NS
NT:
Receptor:
Target:

A

NT: Ach
Receptor: N1
Target: Skeletal muscle

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3
Q

ANS Parasympathetic
Target:

Pre-ganglionic NT:
Pre-ganglionic Receptor:
Post-ganglionic NT:
Post-ganglionic Receptor:

A

Target: SM, cardiac muscle, glands

Pre-ganglionic NT: Ach
Pre-ganglionic Receptor: N2
Post-ganglionic NT: Ach
Post-ganglionic Receptor: M

slows HR

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4
Q

ANS Sympathetic
Target:

Pre-ganglionic NT:
Pre-ganglionic Receptor:
Post-ganglionic NT:
Post-ganglionic Receptor:

A

Target: SM, cardiac muscle, gland

Pre-ganglionic NT: Ach
Pre-ganglionic Receptor: N2
Post-ganglionic NT: norepinephrine and epinephrine
Post-ganglionic Receptor:alpha and beta receptors

inc HR

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5
Q

draw NT, Agonist and antagonist diagram for nicotinic and muscarinic receptors

A

…

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6
Q

Nm and Nn

A

Nm: skeletal muscle
Nn: autonomic ganglia

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7
Q

Usually nicotinic receptors aren’t targeted by drugs, the ones that are however are…

A

Ganglion Blockers: drugs that act as antagonists at Nn. for hypertension

Neuromuscularblockers: antagonists at the Nm receptors > neuromuscular blockade

not very good, muscarinic better!

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8
Q

Main muscarinic drug target

A

Atropine.
Given via injection post heart-attack, to reverse transient in parasympathetic tone.

Increases firing of the SA node and conduction through the AV node

  • dilates pupils
  • inhibits saliva, sweat and mucus gland secretions
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9
Q

Adrenergic Receptors

A

On target tissues for SNA. Alpha and beta adrenergic receptors on postsynaptic cell.

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10
Q

alpha and beta adrenoreceptors

A

2 primary classes of receptors.

Variation in Specificity:
alpha: noradrenaline > adrenaline > isoproteronol

beta: isoproteronol > adrenaline > noradrenaline

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11
Q

B1

A

found mainly in heart, increases rate and force of contraction

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12
Q

B2

A

causes SM relaxation

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13
Q

a1

A

contraction of vascular SM. Increase BP

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14
Q

a2

A

inhibition of transmitter release. On the nerve cell itself, on presynaptic cell, NA binds and has a negative-feedback effect on the NA. SO when there’s excess NA it can be controlled.

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15
Q

a1 agonist

A

phenylephrine (constricts and stops runny nose)

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16
Q

a2 agonist

A

clonidine (drops BP)

17
Q

B1 agonist

A

dobutamine. Inc cardiac contracting

18
Q

B 2 agonist

A

salbutamol - inhalers.

19
Q

Parasympathetic efferent control

A

Controls mainly only HR, via Ach (at SA and AV node), targets the atria.
From cardiovascular control system in medulla

20
Q

Sympathetic efferent control

A

Also from cardiovascular control system in the medulla.

Targets both atria and ventricles, arteries and veins (resistance and capacitance vessels).

21
Q

PS influence on HR

A

Much faster then sympathetic control, within 1 beat.

Strong vagal stimulation can actually stop heart.

The changes in HR per breathe are due to vagal activity as it occurs so quickly,

22
Q

Sympathetic influence on HR

A

Sympathetic stimulation does lead to an increase in heart rate, but at a much slower rate then PS.

23
Q

HR is set by SA node, which has an unstable resting membrane potential “pacemaker potential”. This is set by

A

Balance between If (inward) and I (outward) currents.
Inward current slightly larger

Rapid depol due to transient calcium channel

24
Q

HR will still occur even without neural control. But what happens with vagal and sympathetic stimulation

A

Vagal: ACh hyperpolarizes the membrane potential (more Ik, less If) = slower HR
More negative to start with AND lower slope

Sympathetic: NA increases rate of depol (increases If) = faster HR

25
Q

How is HR affected with a heart transplant

A

No nerves to heart, so even with exercise the sympathetic stimulation cant really occur, so HR doesn’t really rise

26
Q

How does sympathetic control impact SV?

A

Noradrenaline release > acts on B receptors > increased DHPRs Ca release
also acts on SERCA > inc cytosol Ca
Net result = bigger/shorter contraction (inc inotropy)

27
Q

Beta-blockers

A

commonly used in CVD, especially heart failure.

Reduces the amount of work the heart has to do > reduces O2 needs

  • prevent arrhythmias
  • reduce workload in HF
  • reduce BP

meds end in “lol”

28
Q

Efect of sympathetic activity on TPR

A

NOT like a switch, always at a certain level.
Increased > VC > inc resistance

Decreased > VD > dec resistance

29
Q

how do a 1 receptors actually work to cause vasoconstriction?

A

NE > a1 receptors > IP3 (2nd messenger) > Ca release from SR > more contraction

30
Q

how do B2 receptors actually work to cause vasodilation

A

stimulation of B2 receptors > MLCK inhibition > VD

31
Q

Baroreceptors and chemoreceptors are found in …

A

carotid arteries and aortic arch

32
Q

Barorecptor reflex

A

Incr arterial pressure > incr baroreceptor finding > incr in activity to NTS > inc in vagal activity and inhibition of sympathetic nerve activity

This results in decreased HR, SV, and BP (inc VD)

33
Q

CHemoreceptor Reflex

A

Stimuli: hypoxia, , hypercapnia and low pH
Innervation from : sinus (branch of IX) and aortic (branch of X) nerves
Initiated from: carotid and aortic bodies

Reflex effects : inc ventilation and sympathetic VC activity

34
Q

Note on central chemoreceptors

A

ONLY respond to hypercapnia and low pH

35
Q

Diving Reflex

A

O2 conserving response, initiated by water on the face.
Response to
- stimulation of afferent fibres of the 9th cranial nerve
-central comman (voluntary breath hold
-central and peripheral chemoreceptors (pH, pO2, pCO2)

Breath holding (apnea), bradycardia (decr HR due to increase vagal activity)

peripheral VC and rise of BP occurs (inc sympathetic activity

Cardiovascular System (34 decks)

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