Autonomic Control Of CVS Flashcards
What are the divisions of the ANS
• Parasympathetic nervous system - craniosacral origin
• Sympathetic nervous system - thoracolumbar origin
• This division is based on anatomical grounds
- some textbooks include enteric as a 3rd division
What are the fucntions of the autonomic nervous system
- Regulates physiological functions – Examples: BP,
- 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
Is sympathetic drive to different tissues regulated dependently or independently?
Sympathetic drive to different tissues is independently regulated
• eg sympathetic activity to the heart can be increased without increasing
activity to GI tract
• on some occasions (fight or flight) there can be a more co-ordinated
sympathetic response
Describe the autonomic corntol of the CVS
Control of the cardiovascular system • The ANS controls – heart rate – force of contraction of heart – peripheral resistance of blood vessels - heart at rest in normalcy under vagal control - both active at rest but para dominates - if all auto blokefd - heart rate increase o 100-105
• What the ANS does not do
– The ANS does not initiate electrical activity in the heart
• Denervated heart still beats, but at faster rate
• At rest the heart is normally under vagal influence
Describe the parasympathetic input to the heart
• Preganglionic fibres - 10th (X) cranial nerve VAGUS
• Synapse with postganglionic cells on epicardial surface or within
walls of heart at SA and AV node
• postganglionic cells release ACh
• acts on M 2
-receptors
– decrease heart rate (-ve chronotropic effect)
– decrease AV node conduction velocity
Describe the sympathetic input to the heart
Sympathetic input to the heart
• Postganglionic fibres from the sympathetic trunk
• Innervate SA node, AV node and myocardium - ventricles get sympathetic but very little parasympathetic innervation
– Release noradrenaline
• Acts mainly on β1
– increases heart rate (+ve chrontropic effect) adrenoreceptors
– AND increases force of contraction (+ve inotropic effect)
- faster speed of reaction so can beat more rapidly
• Note: β2 and β3 adrenoreceptors are also resent in the heart, but the main effect is mediated by β1 receptors
Describe the autonomic inputs to the heart
See slide
What are the effects of the ANS on pacemaker potentials
sympathetic effect mediated by β1
receptors G-protein coupled receptors Increase cAMP (as)
speeds up pacemaker potential
Faster depolarisation threshold - more HCN
parasympathetic effect mediated by M2 receptors G-protein coupled receptors Increase K+ conductance and decrease cAMP (ai) Slows depolarisation threshold
How does noradrenaline increase force of contraction
• NA acting on β1 receptors in myocardium causes an increase in cAMP -> activates PKA. Pka also stored in san/van
- phosphorylation of L type Ca2+ channels increases Ca2+ entry during the plateau of the AP
- increased uptake of Ca2+ in sarcoplasmic reticulum -more available beat by beat - more available for release when CICR
• Lead to increased force of contraction
What are the ANS effects on vasculature
• most vessels receive sympathetic innervation
– exceptions
• some specialised tissue eg erectile tissue have
parasympathetic innervation
• most arteries and veins have α1 receptors
– coronary and skeletal muscle vasculature also have β2 receptors
What is vasomotor tone
The vasomotor tone is an essential determinant of blood pressure. Vascular resistance is the result of a calculation including vasomotor tone, blood flow and blood viscosity.
Vasomotor tone allows for vasodilation to occur
If sympathetic output decreased an endothelial cellsporduce nitric oxide -> vasodilation
If sympathetic output increased -> vasoconstriction
How does adrenaline affect vessels with beta 2 and alpha 1 adrenoceptors
Eg skeletal muscle, myocardium,liver
• circulating adrenaline has a higher affinity for β2 adrenoceptors than for α1 receptors
• At physiological concentration circulating adrenaline will preferentially bind to β2 adrenoceptors - dilation
• At higher concentrations it will also activate α1 receptors eg pharmacological - constriction
What are the effects of beta 2 and alpha 1 adrenoceptors on vascular smooth muscle?
• Activating β2 adrenoreceptors causes vasodilation
– increases cAMP -> 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
What is excitation contraction coupling
See slide for diagram
Noradrenaline activates a1 receptors gq coupled - PIP2 split into ip3 and dag, ip3 stimulates SER to release Ca2+ (depolarisation also opens VOCCs)
4 Ca2+ bind to calmodulin which then stimulates the myosin light chain kinase
MLCK phosporylates (activates) the myosin light chain
DAG inhibits the MLC phosphatase
MLCP is constitutively (constantly) active and dephosphorylases myosin light chain
B2 receptors which are gs coupled -> adenylate cyclase -> camp -> pka -> inhibits MLCK
What is the role of local metabolites?
• Active tissue produces more metabolites
– e.g. adenosine, K+, H+, increase PCO2
• Local increases in metabolites have a strong vasodilator effect
• All act to vasodilator
• local increase in metabolise mor important than b2 to increase blood flow to skeletall and coronary tissue
• Metabolites are more important for ensuring adequate perfusion
of skeletal and coronary muscle than activation of β2 -receptors
