Lecture 10- Autonomic cardiac control Flashcards
The ANS has important for regulating many physiological functions inc…
HR, BP, body temp etc (homeostasis)
Fight or flight response (stress response)
*Outside voluntary control*
ANS control over specific tissue
Smooth muscle
Exocrine secretion
Rate and force of contraction in the heart
Two divisions (defined by their origin- anatomical grounds)
Parasympathetic- craniosacral origin
Sympathetic- thoracolumbar origin
sympathetic neurones
preganglionic within CNS (short), postganglionic innervates target tissue (long)

parasympathetic neurones
preganglionic (long), post ganglionic neurone are within the target tissue (short)

function of the ANS
Where parasympathetic and sympathetic divisions both innervate a tissue they often have opposite effects
- Sympathetic activity is increased under stress
-
Parasympathetic system is more dominant under basal conditions
- Both work together to maintain balance
sympathetic effect and receptor: pupil of the eye
dilation (contracts raidal muscle)
alpha1
sympathetic effect and receptor: airways of lungs
relax
Beta1
sympathetic effect and receptor: heart
increase rate (chronotropy) and force of contraction (inotropy)
Beta1
sympathetic effect and receptor: sweatglands
localised secretion (e.g. palms)–> alpha1
generalised secretion–> M3
*Sweat glands- one of the only sympathetic receptors that use ACh*
parasympathetic effect and receptor: pupil of eye
contraction (contracts sphincter muscle)
M3
parasympathetic effect and receptor: airways of lungs
contracts
M3
parasympathetic effect and receptor: heart
decrease rate
M2
parasympathetic effect and receptor: sweat glands
no effeect
ANS control of CVS
Heart rate
Force of contraction of heart
Peripheral resistance of blood vessels
what does thr ANS not do to the CVS
Initiate electrical activity in the heart
if the heart was dennervated
Dennervated heart still beats, but at a faster rate
At rest the heart is normally under vagal (parasympathetic) influence
(1) Parasympathetic input of the heart
- Preganglionic fibres- 10th X cranial nerve VAGUS
- Synapse with postganglionic cells on epicardial surface or within the walls of the heart at the SA and AV node
- Slow conduction at both SA and AV
- Post ganglionic release ACh
- Acts on M2 receptors
- Decrease heart rate (-ve chronotropic effect)
- Decrease AV node conduction velocity
(2) Sympathetic input to the heart
- Post ganglionic fibres from the sympathetic trunk
- Innervates SA, AV node and myocardium
- Release noradrenaline
- Acts mainly on B1 adrenoreceptors
- Increases heart rate (+ve chronotropic effect)
- And increases forces of contraction (+ve inotropic effect)
- B2 and B3 also present in heart, but the main effect is mediated by B1 receptors
autonomic NS input into the heart diagram

The pacemaker of the heart
Cells in the SAN steadily depolarise towards threshold
- Slow depolarising pacemaker potential
- Turning on of a slow Na+ conductance-HCN (If-funny current)
- Opening of ca2+ channels
- AP firing in the SA node set the rhythm of the heart

Effects of ANS on the pacemaker potential (chronotropic): sympathetic
effects mediated by b1 receptor
GPCR
- increase cAMP
- speed up pacemaker potential
HCN – cyclic nucleotide gated
–>Increase cAMP, increase If current
Effects of ANS on the pacemaker potential: parasympathetic
effects mediated by M2 receptors
GPCR
- increased K+ conductance
- decrease CAMP
How does NA increase force of contraction? (inotropic)
- NA acting on B1 receptors in myocardium causes an increase in cAMP –> activates PKA (GalphaS)
- Phosphorylation of Ca2+ channels increase Ca2+ entry during the plateau of the AP
- Increase uptake of Ca2+ in SR
- Leads to increased force of contraction





