Autonomic control of CVS Flashcards
what does the ANS exert control over
smooth muscle (vascular and visceral)
exocrine secretion
rate and force of contraction in the heart
how are the pre and pro ganglionic neurones arranged in the SNS & PNS
preganglionic is shorter than post ganglionic in SNS
opposite in PNS, post ganglionic neurone is embedded within tissue it will innovate
what are the functions of the autonomic NS? what are the 2 divisions? and when is there activity increased
regulate physiological functions (BP, heart rate , sweating , bronchodilation)
parasympathetic and sympathetic
sympathetic activity is increased under stress
parasympathetic is more dominant under basal conditions
which neurotransmitter does SNS use
noradrenaline/ adrenaline
which neurotransmitter does parasympathetic use generally
acetylcholine
name some examples of ANS control
airways of lungs: sympathetic effect isn relaxation by b2 receptors. parasympathetic effect is contraction by muscarinic (M3) receptor
heart :SNS causes increased heart rate and contraction by B1 and PNS causes decreased rate by muscarinic (M2) receptor
what control does the ANS have on CVS
heart rate
force of contraction of heart
peripheral resistance of blood vessels
what would happen to the heart rate if you totally denervate the heart
heart still beats but faster heart rate
main ANS supply to the heart is vagus nerve. PNS is active during rest and digest so it slows heart down but when this is taken away there is only the SNS which will speed up the heart.
parasympathetic input to heart
preganglionic fibres - vagus nerve
synapse with postganglionic cells on epicardial surface ore within walls of the heart at SA and AV node
postganglionic cells release ACh that act on M2 receptors.
this decreases the heart rate (-ve chronotropic effect)
decreases AV node conduction velocity as well
sympathetic input to heart
post ganglionic fibres from the sympathetic trunk innervate SA node, AV node and myocardium.
release NA that acts on B1 adrenoreceptors
increase <3 rate (+ve chronotropic effect)
increase force of contraction (+ve inotropic effect)
which part of the heart affects rhythm and which affects force of contraction
SA node affects rhythm and myocardium affects force of contraction
where is the pacemaker of the heart and how does it set a rhythm
cells in the SA node steadily depolarise toward threshold
1)turning on of slow Na+ conductance (Funny current)
2)opening of Ca2+ channels
3)closing of Ca2+ and opening of K+ channels
AP firing in the SA node sets the rhythm of the heart
what receptors is the sympathetic effect on ANS mediated by and what does it do
mediated by B1 receptors (G protein coupled receptor)
increased cAMP
speeds up pacemaker potential
what receptors is the parasympathetic effect on ANS mediated by and what does it do
mediated by M2 receptors(G-protein coupled receptors)
increase K+ conductance and decreases cAMP
How does NA increase force of contraction
NA acting on B1 receptors in myocardium cause an increase in cAMP activating PKA.(protein kinase A)
phosphorylation of Ca2+channels increases Ca2+entry during the plateau of the AP
increased uptake of Ca2+ in SR so more valuable for release from stores
this leads to increased force of contraction
what receptors do most vasculature have
a1-adrenoreceptors
coronary and skeletal muscle vasculature also have B2-receptors
how is vasodilation/vasoconstriction controlled
vasomotor tone
there is no parasympathetic output so it is controlled by changing the levels of sympathetic output
vasodilation is decreased sympathetic output
by having a basal level tone, both dilation and constriction can occur.
in blood vessels with both b2 and a1 adrenoceptors what is the response to adrenaline
circulating adrenaline has a higher affinity for b2 adrenoreceptors. however when circulating adrenaline has increased for example in exercise or fight/flight response adrenaline will also activate a1 receptors
what does activation of B2 adrenoreceptors in vascular smooth muscle cause
vasodilation
as it increases cAMP activating PKA, opening up potassium channels and inhibiting MLCK. inhibition of this brings about relaxation as muscle contraction is inhibited.
what does activation of a1 adrenoreceptors in vascular smooth muscle cause
vasoconstriction
stimulates IP3 production.
increase in [Ca2+]in from stores and via influx of extracellular Ca2+ leading to contraction of smooth muscle
role of local metabolites in vsm
active tissues produce more metabolites which have a strong vasodilator effect
where are baroreceptors located and what do they detect
they are stretch receptors
located in aortic arch and carotid sinus
detect increased BP and stretch more
what is given during anaphylactic shock
adrenaline
higher conc given so it activates a1 receptor overcoming b2 effects
name a b1 agonist and what its used for
dobutamine cariogenic shock (pump failure)
name a b2 agonist and what it treats
salbutamol
asthma
what do a adrenoceptor antagonists do and give an example
prazosin
anti hypertensive agent
inhibits NA causing vasodilation
not first line therapy
what does propranolol do what type of drug is it and what could be used instead
b adrenoceptor antagonist non selective on b1 and b2 slows heart rate and reduces force of contraction (b1) but bronchoconstriction too- b2 atenolol is selective
name a muscarinic agonist, what does it do
pilocarpine
treats glaucoma
activates constrictor pupillae
improves drainage of aq humour
name a muscarinic antagonist, what does it
atropine/ tropicamide
increase <3 rate and bronchial dilation
used to dilate pupils for examination of the eye
