Autonomic Control Flashcards
What activity is up is cardiovascular disease
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
Somatic NS
NT:
Receptor:
Target:
NT: Ach
Receptor: N1
Target: Skeletal muscle
ANS Parasympathetic
Target:
Pre-ganglionic NT:
Pre-ganglionic Receptor:
Post-ganglionic NT:
Post-ganglionic Receptor:
Target: SM, cardiac muscle, glands
Pre-ganglionic NT: Ach
Pre-ganglionic Receptor: N2
Post-ganglionic NT: Ach
Post-ganglionic Receptor: M
slows HR
ANS Sympathetic
Target:
Pre-ganglionic NT:
Pre-ganglionic Receptor:
Post-ganglionic NT:
Post-ganglionic Receptor:
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
draw NT, Agonist and antagonist diagram for nicotinic and muscarinic receptors
…
Nm and Nn
Nm: skeletal muscle
Nn: autonomic ganglia
Usually nicotinic receptors aren’t targeted by drugs, the ones that are however are…
Ganglion Blockers: drugs that act as antagonists at Nn. for hypertension
Neuromuscularblockers: antagonists at the Nm receptors > neuromuscular blockade
not very good, muscarinic better!
Main muscarinic drug target
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
Adrenergic Receptors
On target tissues for SNA. Alpha and beta adrenergic receptors on postsynaptic cell.
alpha and beta adrenoreceptors
2 primary classes of receptors.
Variation in Specificity:
alpha: noradrenaline > adrenaline > isoproteronol
beta: isoproteronol > adrenaline > noradrenaline
B1
found mainly in heart, increases rate and force of contraction
B2
causes SM relaxation
a1
contraction of vascular SM. Increase BP
a2
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.
a1 agonist
phenylephrine (constricts and stops runny nose)
a2 agonist
clonidine (drops BP)
B1 agonist
dobutamine. Inc cardiac contracting
B 2 agonist
salbutamol - inhalers.
Parasympathetic efferent control
Controls mainly only HR, via Ach (at SA and AV node), targets the atria.
From cardiovascular control system in medulla
Sympathetic efferent control
Also from cardiovascular control system in the medulla.
Targets both atria and ventricles, arteries and veins (resistance and capacitance vessels).
PS influence on HR
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,
Sympathetic influence on HR
Sympathetic stimulation does lead to an increase in heart rate, but at a much slower rate then PS.
HR is set by SA node, which has an unstable resting membrane potential “pacemaker potential”. This is set by
Balance between If (inward) and I (outward) currents.
Inward current slightly larger
Rapid depol due to transient calcium channel
HR will still occur even without neural control. But what happens with vagal and sympathetic stimulation
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
How is HR affected with a heart transplant
No nerves to heart, so even with exercise the sympathetic stimulation cant really occur, so HR doesn’t really rise
How does sympathetic control impact SV?
Noradrenaline release > acts on B receptors > increased DHPRs Ca release
also acts on SERCA > inc cytosol Ca
Net result = bigger/shorter contraction (inc inotropy)
Beta-blockers
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”
Efect of sympathetic activity on TPR
NOT like a switch, always at a certain level.
Increased > VC > inc resistance
Decreased > VD > dec resistance
how do a 1 receptors actually work to cause vasoconstriction?
NE > a1 receptors > IP3 (2nd messenger) > Ca release from SR > more contraction
how do B2 receptors actually work to cause vasodilation
stimulation of B2 receptors > MLCK inhibition > VD
Baroreceptors and chemoreceptors are found in …
carotid arteries and aortic arch
Barorecptor reflex
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)
CHemoreceptor Reflex
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
Note on central chemoreceptors
ONLY respond to hypercapnia and low pH
Diving Reflex
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
