Autonomic Control of the CVS Flashcards
Give some examples of ANS control, stating the receptors used
Pupil of eye - symp = dilation (alpha 1), para = contraction (muscarinic 3)
Airways of lungs - symp = relax (beta 2), para = contract (muscarinic 3)
Heart - symp = +ve inotropic and +ve chronotropic (beta 1), para = -ve chronotropic (muscarinic 2)
Sweat glands - symp = localised scretion (alpha 1) and generalised secretion (muscarinic 3)
What does the ANS control in the CVS and which nerve innervates the heart
Heart rate
Force of contraction
Peripheral BV resistance
Heart is innervated by vagus nerve
How does the parasympathetic NS control the heart - nerve, what it affects, what it releases, what it does
Vagus nerve (preganglionic fibres)
Synpases at SA and AV node and cells on epicardial surface
Release ACh
Act on M2 causing -ve chronotropic effect and decreased AV node conduction velocity
How does the sympathic NS control the heart - nerve, where and what it innervates, effect on heart
Postganglionic fibres from sympathetic trunk
Innervate SA and AV node, and ventricular myocardium
Beta 1 adrenoceptors - +ve chronotropic and +ve inotropic effect, speeds up relaxation of heart
What is the SNS affect on the pacemaker potential and how does it come about
Increases the slope, speeding up depolarisation
Beta 1 receptors produce alpha-S subunit which then causes an increase in cAMP which can open HCN channels, allowing for faster depolarisation
What is the PSN affect on pacemaker potential and what is its mechanism
Decreaes the slope, slowing down depolarisation
M2 receptor produces alpha-I subunit which inhibits cAMP production. There is an increase K+ conductance and decreased cAMP so the potential slows down
Describe the effects of the ANS on the vasculature - when the output is normal, increased and decreased
Normal - some NA acts on alpha-1 receptors to allow some vasoconstriction to occur creating a vasomotor tone
Increased - increased NA release causes vasoconstriction of vessels
Decreased - decreased NA release causes less vasoconstriction resulting in vasodilation
What do Beta-2 receptors on vessels cause
Vasodilation
How does adrenaline go from causing vasodilation to causing vasoconstriction
Physiological concentration of adrenaline has higher affinity for B2 then A1 so will bind to B2 causing vasodilation
Higher concentrations of adrenaline will also bind to A1 causing vasodilation
How do B2 adrenoreceptors cause vasodilation
Increases cAMP, activating PKA, opening K+ channels and inhibiting MLCK causing relaxation of SM
How do A1 adrenoceptors cause vasoconstriction
Stimulates IP3 production, increasing [Ca2+]in from stores and extracellular influx, causes contraction of smooth muscle
What is the role of local metabolites in the vasculature
Metabolites cause vasodilation
Very important for ensuring adequate perfusion of skeletal and coronary muscle
What are the sensory receptors of CVS
Baroreceptors and atrial receptors
What are and how do baroreceptors work (what nerves do they communicate with)
They are nerve endings in carotid sinus and aortic arch sensitive to stretch
Increased arterial pressure stretches receptors causing a lot of feedback to be send to CV centre, so the CV centre responds with vasodilation
Glossopharyngeal and vagus nerve
Name some sympathomimetics and their uses
Adrenaline - restore function in cardiac arrest, administered for anaphylactic shock
Dobutamine - B1 agonist, give in cardiogenic shock, causes +ve inotropic affect
Salbutamol - B2 agonist, treatment of astham, relaxation of bronchial SM
