Flashcards in 4. Autonomic control of the CVS Deck (20)
What are the 2 parts of the ANS, what is this division based on, and when is each division dominant?
Based on anatomical grounds:
- sympathetic (thoracolumbar origin): increased under stress
- parasympathetic (craniosacral origin): dominant under basal conditions
Both work together to maintain homeostasis.
Is sympathetic drive to different tissues independently regulated or co-ordinated?
Independently, though can be a more co-ordinated response on some occasions (fight or flight)
What components of the CVS does the ANS control?
1. heart rate (chronotropy)
2. force of contraction of heart (inotropy)
3. peripheral resistance of blood vessels (arteriolar contraction)
At rest, which part of the ANS controls the heart rate?
Parasympathetic (denervated heart beats at faster rate)
Describe the components (nerves, NT and Rs) involved in parasympathetic input to heart.
- Preganglionic fibres (Xth 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 M2-receptors
What are the effects of parasympathetic and sympathetic stimulation of the heart?
- decrease heart rate (-ve chronotropic effect)
- decrease AV node conduction velocity
- increase heart rate (+ve chronotropic effect)
- increase force of contraction (+ve inotropic effect)
Describe the components (nerves, NT and Rs) involved in sympathetic input to heart.
- Postganglionic fibres from sympathetic trunk innervate SA node, AV node and myocardium.
- Release noradrenaline.
- Acts mainly on B1 adrenoreceptors.
How are changes in heart BP sensed and regulated by the ANS?
1. Baroreceptors in the carotid sinus and aortic arch measure arterial BP.
2. Signal to cardiovascular center in medulla oblongata via glossopharyngeal nerves (cranial nerve IX).
3. CV center regulates BP via vagus nerve (cranial nerve X, parasympathetic) and cardiac accelerator nerve (sympathetic).
Describe the effects of the sympathetic NS on pacemaker potential/chronotropy. How is this mediated by the relevant receptors?
Speeds up pacemaker potential: increases slope... reach threshold sooner... APs fire closer together.
1. Sympathetically released NA activates B1 Rs.
2. Galpha s stimulation results in increased [cAMP]... enhances opening of HCN channels.
4. Speeds up pacemaker potential.
Describe the effects of the parasympathetic NS on pacemaker potential/chronotropy. How is this mediated by the relevant receptors?
Slows pacemaker potential: decreases slope... slower to reach threshold... reduced AP firing.
1. Parasympathetically released ACh activates M2 Rs.
2. Galpha i stimulation results in in decreased [caMP]... inhibits opening of HCN channels.
3. Gbeta/gamma i opens K+ channels... increases membrane potential.
4. Slows pacemaker potential.
How does noradrenaline increase contraction force (inotropy)?
NA activates B1 Rs in myocardium... increased in cAMP... activates PKA.
1. PKA phosphorylates Ca2+ channels... increased Ca2+ entry during AP plateau.
2. Increased Ca2+ uptake in sarcoplasmic reticulum at rest - greater store.
3. Increased sensitivity of contractive machinery to Ca2+.
Which division of the ANS innervates the vascular system? What type of NT receptor is present here?
- Most BVs innervated by sympathetic NS (exception: some specialised tissues, e.g. erectile tissue, have parasympathetic innervation).
- Most arteries and veins have alpha1-adrenoreceptors; coronary and skeletal muscle vasculature also have beta2-adrenoreceptors.
What is vasomotor tone and what does this allow?
- Vasomotor tone = basal level of sympathetic NS activity - certain amount of arteriolar smooth muscle contraction.
- vasodilation (decreased sympathetic output)
- vasoconstriction (increased sympathetic output)
What are the effects of B2 and a1 adrenoR stimulation on vascular smooth muscle?
Activating B2 Rs causes vasodilation
- increases cAMP... PKA... opens K+ channels (hyperpolarisation so decreased Ca2+ influx) and inhibits MLCK... SM relaxation.
Activating a1 Rs causes vasoconstriction
- stimulates IP3 production... increases [Ca2+]i from stores and via influx of extracellular Ca2+... SM contraction.
Why does adrenaline has opposite effects on vasomotor tone at physiological and increased concentration?
- Circulating adrenaline has higher affinity for B2 adrenoRs (in BVs of skeletal muscle, myocardium and liver) than for a1 adrenoRs.
- At phyisological concentration, circulating adrenaline preferentially binds to B2 adrenoRs - causes vasodilation.
- At higher concentrations, adrenaline also activates a1 adrenoRs - causes vasoconstriction.
What is the main process causing vasodilation?
Active tissues (i.e. cardiac and skeletal muscle during exercise) produce more metabolites... local increase in metabolites has strong vasodilatory effect.
Metabolites are more important for ensuring adequate perfusion of skeletal and cardiac muscle than B2 R activation.
Describe in general terms how changes in the state of the CVS (e.g. change in BP) are communicated to the brain and the response this will cause.
1. Baroreceptors (high pressure side of system) and atrial receptors (low pressure side of system) signal to medullary CV center via afferent nerves.
2. CV center alters activity of efferent nerves to heart and BVs.
What are baroreceptors?
Are nerve endings in the carotid sinus and aortic arch that are sensitive to stretch, i.e. from increased arterial pressure.
Which nerves communicate signals from the baroreceptors to the medullary CV center?
- Carotid sinus baroreceptors innervated by branch of glossopharyngeal nerve.
- Aortic arch baroreceptors innervated by branch of vagus nerve.