CVS 10 - Autonomic control of the CNS Flashcards
Describe the functions of the ANS
What does the ANS exert control over?
How is the ANS divided?
- Regulates physiological, non-voluntary functions (e.g.: HR, BP, sweating etc).
- Exerts control over SM, exocrine secretions, rate and force of the heart.
- Into the sympathetic + parasympathetic, based on where they arise from the CNS (SNS = T1-L2, PNS = medullary + sacral)
Describe the arrangement of pre and post-ganglionic ANS neurones.
- Sympathetic has short preganglionic, ganglion within the CNS, longer postganglionic.
- Parasympathetic has longer preganglionic, ganglion close to or within target tissue.
- Both release ACh from preganglionic acting on nAChR’s, SNS releases NA at postganglionic, PNS releases ACh at postganglionic acting on mAChR’s.
What 3 things does the ANS regulate in the cardiovascular system?
What does the ANS not do in the CVS?
- 1) HR 2) Force of contraction 3) Peripheral resistance of blood vessels.
- ANS does not initiate electrical activity.
- Denervated heart still beats, but at slower rate as heart is under vagal influence at rest.
Describe the anatomy + effects of parasympathetic input to the heart.
Describe the anatomy + effects of sympathetic input to the heart.
- Preganglionic fibres (10th cranial nerve/vagus nerve) synapse with postganglionic cells at the SAN + AVN. Postganglionics release ACh to act on M2 receptors (decrease HR + AV node conduction velocity).
- Postganglionics come from sympathetic trunk, innervate the SAN, AVN + myocardium. Releases NA acting on B1-Adr’s (increases HR + force of contraction).
What are the effects of PNS + SNS input on the pacemaker potentials in SAN (pacemaker) cells? (i.e.: how does the ANS increase/decrease HR?)
- SNS exerts effect via B1-Adr’s (Gs coupled), binding of NA increases cAMP. Pacemaker potential a result of funny current (carried by HCN channels). As cAMP is a cyclic nucleotide, it increases their activation and funny current - PP slope increases/PP speeds up.
- PNS exerts effects via M2 receptors (Gi coupled). Gi increases K+ conductance and decreases cAMP. Less activation of HCN channels, decreasing funny current - PP slope decreases/PP slows down.
NB: this is how ANS speeds up/slows down HR.
How does NA from the SNS increase force of contraction in the heart?
1) NA binds to B1-Adr’s in myocardium, causes increase in cAMP + activation of PKA
2) PKA PP’s Ca2+ channels to increase Ca2+ entry during plateau phase
3) Leads to increased uptake of Ca2+ in SR so more Ca2+ available for release from CICR stores.
4) More Ca2+ = increased force of contraction.
- PKA also PP’s phospholamban which regulates Ca2+ ATPase in SR - PP causes increased uptake into SR as it phospholamban no longer inhibits SERCA
What kind of innervation do most vessels receive?
How does vasomotor tone allow for vasodilation/vasoconstriction to occur?
- Most vessels receive sympathetic innervation, most arteries and veins have a1-adr’s.
- The normal sympathetic output to vessels is called the basal vasomotor tone. This allows for a decrease in sympathetic output to cause vasodilation and an increase in sympathetic firing to cause vasoconstriction.
What other receptors do some blood vessels possess? (give examples)
How will this affect vessel width?
- Some vessels (skeletal muscle, myocardium + liver) possess B2-Adr’s as well as a1-Adr’s.
- Circulating AD binds preferentially to these B2-Adr’s, which mediate vasodilation at physiological concentrations.
- At higher concentration of AD, it can also activate some a1-Adr’s.
What is the effect of activating B2 + a1-ADR’s on vascular smooth muscle?
How are these effects exerted?
- Activating B2-Adr’s causes vasodilation - increases cAMP (Gs linked) –> PKA –> K+ channel open –> Inhibits MLCK –> relaxation of SM.
- Activation a1-Adr’s causes vasoconstriction - stimulates IP3 production (Gq linked), increase in IC Ca2+ –> contraction of SM.
How do local metabolites ensure adequate perfusion of skeletal and coronary muscle?
- Active tissues produce metabolites (adenosine, K+, H+ etc)
- They have strong vasodilator effect
- This is a more important factor for perfusion than activation of B2-Adr’s.
How does the baroreceptor reflex communicate changes in BP?
- Baroreceptors are nerve endings found in the carotid sinus and aortic arch, which are stretch sensitive.
- Increase arterial BP = increased stretch = increased AP firing to the brain steam.
- This causes inhibition of SNS to heart + vessels and increases activation of PNS to heart.
- Result is bradycardia + vasodilation to decrease MAP.
NB: Vice versa for decreases in MAP.
Are baroreceptors responsible for maintaining BP in the short or long term?
- Short-term, compensating for moment to moment changes in arterial BP.
- They can reset to higher levels with persistent increases in BP … so cant control long term.
Give examples of sympathomimetics + their cardiovascular uses.
- Adrenaline - administered to restore function in cardiac arrest and anaphylactic shock.
- Dobutamine - B1 agonist given in cardiogenic shock.
- Salbutamol - B2 agonist in treatment of asthma
Give an example + use of an a-adr and b-adr antagonist
- a1-antagonist prazosin = anti-hypertensive, inhibits NA action on vascular SM to cause vasodilation.
- non-selective b-adr antagonist = propranolol, blocks action of NA at b-adr’s to reduce HR and force of contraction. (also causes bronchoconstriction as its non-selective and acts on B2-adr’s).
Give an example and use of a muscarinic agonist + antagonist (cholinergics).
Agonist = pilocarpine, treats glaucoma, activates constrictor pupillae muscle to improve drainage of aqueous humour.
Antagonist = atropine, increases HR + causes bronchial dilation.
