ANS Regulation of the Cardiovascular System Flashcards
Afferent
transmits sensory information from peripheral organs to the CNS
Efferent
carry motor information away from the peripheral nervous system to the muscles, heart, blood vessels, and glands
Somatic
ACh/Nicotinic receptor (skeletal muscle)
Sympathetic
ACh/Nicotinic receptor –> Norepinephrine/alpha1, 2, beta1, 2 adrenergic receptors
alpha1 g-coupled + norepinephrine
vasoconstriction
alpha2 g-coupled + norepinephrine
auto-inhibitory
beta1 g-coupled + norepinephrine
heart (increase in heart rate and stroke volume)
beta2 g-coupled + norepinephrine
vasodilation
Parasympathetic
ACh/Nicotinic Receptor –> ACh/Muscarinic Receptor
Sympathetic/Adrenal
ACh/Nicotinic Receptor –> Adrenal Medulla –> Epinephrine (80%) and Norepinephrine (20%)
Sympathetic Nervous System helps us
handle life’s stresses: hemorrhage, exercise, or even a change in posture
Parasympathetic Nervous System helps us
conserve and store energy
Anatomy (sympathetic)
thoraco-lumbar
Anatomy (parasympathetic)
cranio-sacral
Sympathetic functions
dilate pupils, dilate bronchioles, increase HR and SV, release adrenaline/epinephrine, stop digestion, delay emptying colon and bladder, stress: fight or flight
Parasympathetic functions
constrict pupils, constrict bronchioles, decrease HR, promote digestion, empty colon and bladder, rest and recovery
Atropine blocks
muscarinic receptors
propanolol blocks
beta1 receptors
Vagus dominates at
rests
sympathetic dominates during
exercise
Parasympathetic changes in HR are
fast
Sympathetic changes are
slower, increase rate of depolarization
Sympathetic postganglionic fibers
NE released onto beta1 adrenergic receptors: HR^
Parasympathetic (vagus) postganglionic fibers
release ACh onto muscarinic receptor: HR decreases
Sympathetic dominates
during exercise
Parasympathetic dominates
at rest
Sympathetic innervation of blood vessels
lots
Parasympathetic innervation to blood vessels
very little
Sympathetic on heart and blood vessels
Cause large increase in HR and SV because increase rate, contractility, relaxation, conduction velocity
Increase in TPR (increase in arterial constriction), and decrease in compliance (increase in venous constriction)
Parasympathetic on heart and blood vessels
Cause large decrease in HR due to decrease in rate and conduction velocity
Little change to blood vessels because little change to arterial and venous constriction
Sympathetic: stress
increase HR, SV –> increase CO
ensure blood flow to heart and brain
regulates heart rate during exercise
innervates blood vessels throughout the body
Parasympathetic: recovery
rest and relaxation: decrease HR
Promotes digestion
Regulates HR at rest
Primarily vagus (heart); limited blood vessel innervation
Negative feedback control for humans
Control of mean arterial blood pressure
Two advantages of using a negative feedback control system for mean blood pressure
if CV system starts to fail can compensate, can fix a disturbance
Cut the baroreceptor nerves
brainstem does not know the real blood pressure
R = set point
= 100 mmHg
G = cardiovascular system
= heart, arteries and arterioles, veins and venules
H = baroreceptors
= carotid sinus and aortic = afferent nerves
D = disturbance
= hemorrhage, exercise
Pa = mean arterial pressure
try to keep at 100 mmHg
Between MAP and receptor firing rate around 100 mmHg (zone of maximal sensitivity)
Linear relationship
Baroreceptors are
stretch receptors, when MAP ^, the afferent nerve firing ^
With no baroreflex (open loop)
H = 0, deltaPa = deltaD
Linear, time-invariant system, look at changes in Pa
Pa = (D/(1+GH)) + ((RG)/(1+GH))
If no disturbance
deltaD = 0
If there is no change in our set point or th cardiovascular system
delta(RG) = 0
If we get rid of our feedback system (cut the baroreceptor nerves –> open loop)
H = 0
Arterial pressure (Pa) decreases
decrease in baroreceptor nerve firing
decrease in baroreceptor firing
e>0
e>0
increase in sympathetic firing, decrease in parasympathetic firing
increase in sympathetic firing
increase in HR, SV, TPR, decrease in Cv
Decrease in parasympathetic firing
increase in HR
Increase in HR, SV, TPR, decrease in Cv
Increase in CO = HR*SV
Increase in CO = HR*SV
Increase in arterial pressure (Pa = CO*TPR)
Control the carotid sinus pressure (CSP)
independently of the mean arterial pressure (MAP)
Open loop:
the carotid sinus is surgically isolated, CSP does not equal Pa
Open loop math
GH = -deltaPa/deltaCSP
GH = -output/input
GH = slope
When CSP is very low
Pa increases
When CSP is very high
Pa decreases
Sympathetic firing increase
Increase in HR, SV, CO, TPR, PA, decrease in Cv –> handle stress, fight or flight
Parasympathetic firing increase
Decrease in HR, CO, Pa, tidal volume, increase in digestion –> rest and recovery
Reflexive (respond to a change in MAP)
gravity, mild exercise
Anticipatory (prevent a change in MAP)
exercise, long term adjustments (pregnancy)
Gravitational changes cause blood to pool in the legs
reduces carotid sinus pressure, activates the baroreflex, HR increases and constrict blood vessels (Cv decreases) –> increase in CO and TPR and therefore Pa
What happens to a swimmer’s heart rate in the “head down” position prior to a race
Pressure at carotid baroreceptors increases when we put our head down (due to gravity), firing of baroreceptor nerves increases, brainstem measures pressure as too high and sympathetic firing decreases –> HR and Blood pressure decreases
Baroreceptors reduce
variability of the blood pressure – no effect on MAP
We have maximum baroreceptor sensitivity near
normal arterial pressure
What happens with hypertension?
Decrease sensitivity (would not respond as well to postural changes, hemorrhage, etc), instead our body adapts to the higher pressure so that we can maintain our sensitivity
With hypertension
curve shifts to the right
Long term blood pressure control involves
hormones (ADH, aldosterone, ANG II), kidney –> gain = infinity
deltaPa = 0
After a heart transplant, which of the following are true?
Circulating epinephrine increases HR by activating beta1 receptors
