Lecture 7 Neural Control

From Iusmphysiology

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===Short  Term Sensor Systems for Neural Regulation===
===Short  Term Sensor Systems for Neural Regulation===
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*This is moment to moment regulation.
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*CV system can respond very quickly.
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*How does it know?
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====Peripheral Arterial Baroreceptors====
====Peripheral Arterial Baroreceptors====
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  Arch of aorta and bifurcation area of common carotid arteries  
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*The first two lines of defense are baroreceptors:
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*Baroreceptors are found in the arch of aorta and the bifurcation area of common carotid arteries in the neck
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  1.  Monitor stretch of vessel         walls
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*Mixed into wall of vessel
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  a.  Vessel wall must deform to
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*Associated with smooth muscle cells
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    generate signal
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*As diameter gets larger, the baroreceptors fire
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  b.  Firing rate proportional to            stretch caused by          pressure
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*They sense tension of themselves too and will fire
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  c.  Carotid baroreceptor  
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*As BP goes up they fire faster and faster
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    (1) glossopharyngeal  nerve  
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*Carotid baroreceptor is
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    (2) Works at pressures of          50-  200 mmHg
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**innervated by glossopharyngeal  nerve  
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    d.  Aortic baroreceptor
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**It is the main receptor becasue it works over a wider range
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    (1) Uses vagus nerve
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*Aortic arch receptor
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    (2)  Works at pressures of                100-200 mmHg
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**Vagus
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**Only over pressures over MAP; stops working over 100 mmHg
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**Can signal when the pressure drops under 100 to tell the brain pressure is low
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BARORPTR
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=====Baroreceptor function=====
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*How do they work?
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*Mechanosensitive Na and Ca channels
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*Ions rush in
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*More depolarization, the faster the signal to the brain trhough glosso and vagus nerves
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=====Influences on baroreceptor function=====
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Diameter of Baroreceptor Vessel
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*This firing is influenced by things in our bodies like abnormal lipid levels, normal or abnomral production of prostacyclins and NO, etc.
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F I    R R  A I    T N  E G
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*Prostacylins and NO (vasodilators):
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**When smooth muscles relaxed, there is more tenstion on the barorecptors because there is more tension
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**So baroreceptors fire
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2.
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**This is good because sympathetics should calm when pressure is going up.
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How Might a Baroreceptor Work at the cellular level?        a.  Mechanosensitive Receptor              1.  Sodium channel allows Na+ ions to enter and partially depolarizes neuron              2.  Likely a calcium channel is opened to allow calcium channels to enter and both depolarize membrane and excite other channels        b.  Near the stretch sensitive site, the local depolarization initiates an action potential that is then propagated.   
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*When lipids are high:
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**Too much LDLs
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**endothelial cells aren't healthy, don't make NO or prostacyclins
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**So we don't get relaxation of smooth muscle
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Likely Modifiers of Function 1.
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**We don't get baroreceptor stretch
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Prostacyclin – increased firing
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**We don't get sympathetic inhibition
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**Blood pressure rises as sympathetics keep signaling smooth muscle to flex and narrow arteries
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2.
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*Platelet activation:
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Nitric Oxide – increased firing
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**Usually act as vasoconstrictyors
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**BAroreceptors are inhibited
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3.
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**Parasympathetics are signaled to fire
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Lipid Abnormality – less firing
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**Body thinks blood pressure is going up but it isn't
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4.
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Activated platelets – less firing
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Ventricular and atrial Baroreceptors
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====Low pressure baroreceptors====
====Low pressure baroreceptors====
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  1. Atria baroreceptors
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*There are baroreceptors in the heart.
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  (a). Atrial Type A - atrial contraction
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**They can cause increase or decrease of neural stimulation at the heart.
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  (b)  Atrial Type B – atrial filling during ventricular systole!! 
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*Atrial Type A baroreceptors:
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  (c) if overactive, suppress antidiuretic hormone release (water        loss), decrease sympathetic activity
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**These monitor atrial contract; tell the brain if it is going well or not.
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  2. Ventricular centers monitor both stretch of ventricle during        diastole and somehow monitor pressure developed.           Hyperactivity  suppresses sympathetic nervous system 
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*Atrial type B
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**Sense how venous pressure is stretching the atrium.
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**Brain stops getting signal if not stretching correctly.
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*Ventricular receptors
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**These sense how well the ventricle is being passively stretched.
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*Different ventricular receptors
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**Detect tension generated during systole
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*If Atrial type a or b are over active, brain is told that atria are doing too much (too much stretch in diastole, or something)
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**Antidiuretic hormone is suppressed to reduce blood volume.
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**Sympathetic activity will also be suppressed.
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*If too much ventricular activit / stretch is detected:
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**Symnpathetic activity is decreased.
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**These are more important than the atrial baroreceptors.
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**Renal lectures will tell us about how atria can release hormones to talk to the kidneys, too.
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Ventricular and atrial Baroreceptors
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===Integration of Input and Output Neural Signals in the Medulla Excitatory Centers===
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*Higher the bp pressure, more firing of baroreceptors.
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*This is a '''reciprocal innervation system''': the more the baroreceptors fire, the more they inhibit cardiac excitatory systems (in the brain stem).
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**Brain stem is generally where sympathetics originate.
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===Integration of Input and Output Neural Signals in the Medulla Excitatory Centers===
 
====Pressor Center - sympathetic  nervous system to blood vessels====
====Pressor Center - sympathetic  nervous system to blood vessels====
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*The pressor center is part of the sympahetics.
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*It talks to the blood vessels
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*When inhibited, less activity to the arteries so they are less constricted.
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*Tries to bring bp up through: venus constriction, arterial constriction, increased heart contractility
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  1. Tonically active but depressed by  baroreceptor input    2. Causes increased arterial resistance and venous constriction   
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====Cardiac inhibitory center====
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Neural control centers and cvtree
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*This is the beginning of the parasympathetics.
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*When these fire, the vagus nerve gets stimulated
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*Vagus goes to SA node, AV node and slows the heart rate
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**Most effective at SA node but also at AV node.
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*Notice that vagus does not (nor does any of the parasymp) affect blood vessels.
====Cardiac Excitatory Center - sympathetic nervous system to heart====
====Cardiac Excitatory Center - sympathetic nervous system to heart====
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*The sympthetic system is tonically active.
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**it must be inhibited or it will fire very fast.
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**Baroreceptors are all calming the parasymp down.
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  1.  Tonically active - but depressed by baroreceptor  input  2.  Increases heart rate and contractility 
 
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Neural control centers and cvtree
 
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Inhibitory Centers
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====Overall outcome of the baroreceptor and central nervous system interaction====
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A.  Depressor Center - suppresses activity of the sympathetic nervous       system to blood vessels
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*As baroreceptor activity is increased, the medulla will reflexively decrease the sympathetic nervous system activity; vagal activity usually changes in the opposite direction of sympathetic activity.
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  1.  Activated by the baroreceptor input
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*The cardiovascular system without sympathetic or parasympathetic activity:
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  2.  Does not send neurons to blood vessels  
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**Heart rate about 100-110 beats/min,
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B.  Cardiac Inhibitory Center
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***SA node has an inherent rate of about 100, so as we rest, parasympathetics dominate HR control (ach > ne)
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  1.  Activated by the baroreceptor input
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**Arterial pressure 65/40 mmHg,
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  2. Vagal activity to the heart to slow the heart rate 
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***pretty low
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**Cardiac output about 70% of normal,
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***Need sympath NE to generate proper heart contraction
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**Vasculatures very dilated,
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***need sympath NE to keep vessels a little constricted
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**Skin warm,
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**mucus membranes flushed,
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**very little tolerance to sitting or standing
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***Because of low cardiac output
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*The Full Neural Control System:  
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**Heart rate should be 70-80 beats / min,
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**arterial pressure 120/70 mmHg,
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**cardiac output 70 ml/min per kg,
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**skin cool and
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**mucus membranes pink,
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***not too much blood flow to the skin
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**able to perform to the maximum ability of the skeletal muscle system.
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Neural control centers and cvtree
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===Modifications of Neural Control By Higher Brain Centers===
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*This is the conscious brain working on our unconscious systems.
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Baroreceptor  and sympathetic activity
 
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The overall outcome of the baroreceptor and central nervous system interaction is  1.  As baroreceptor activity is increased, the medulla will reflexively decrease the sympathetic nervous system activity  2.  Vagal activity usually changes in the opposite direction of sympathetic activity.    The cardiovascular system without sympathetic or parasympathetic activity:  Heart rate about 100-110 beats/min, Arterial pressure 65/40 mmHg, Cardiac output about 70% of normal, Vasculatures very dilated, Skin warm, mucus membranes flushed, very little tolerance to sitting or standing  The Full Neural Control System:  Heart rate should be 70-80 beats.min, arterial pressure 120/70 mmHg, cardiac output 70 ml/min per kg, skin cool and mucus membranes pink, able to perform to the maximum ability of the skeletal muscle system.   
 
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===Modifications of Neural Control By Higher Brain Centers===
 
====Emotion====
====Emotion====
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  1. Pleasurable sensations     Lowers sympathetic activity    Raises vagal activity    Heart rate and pressure fall 
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*Pleasurable sensations
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P1010003
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**BP goes down
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FIRST DINNER PRAYER
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**People who pet dogs or have pets brings down bp.
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**Pleasure lowers sympathetic and increases parasympathetic activity
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  2.  Anger or rage: One of the most potent excitatory mechanisms    for  sympathetic activity        a.  Acts in brain – higher conscious centers increase firing rate of         sympathetic neurons, suppress parasympathetic neurons              b.  Decreased sensitivity of baroreceptors due to their contraction?
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*Anger
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picrdata
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**Excites the sympathetics
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**Acts in the brain, increase firing rate of sympathetic neurons
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  3.  Fear and depression: Inhibits sympathetic activity
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**Can be so potent as to cause an heart attack
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            a.  Works from conscious centers in brain – some how            depresses the medulla
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**Anger also decreases sensitivity of the baroreceptors
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    b.  Sympathetic system depressed, parasympathetic system         activated  - slow heart rate and low vascular resistance  
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*Fear and depression
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**Inhibits sympathetic activity
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cobra
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**Works from conscious centers in brain
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John and Diane's home
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**There is a depression of the sympathetics in the medulla
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**There is a stimulation of the parasympathetic system; this can cause fainting because of the slowed heart rate and low vascular resistance.
====Pain====
====Pain====
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*Sharp pain - activate sympathetic system
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**jazzes up the sympathetics
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*Visceral pain - suppress sympathetic system
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**Childbirth, kidney stone, hit in the chest in car accident
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    1.  Sharp pain - activate sympathetic system    2. Visceral pain - suppress sympathetic system  C.  Exercise   1.  Activate sympathetic nervous system    2.  Emotional connotation  greatly impacts degree of  activation
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====Exercise====
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runner
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*Just knowing you're going to exercise causes increase in sympathetic activity
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m3a
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*The more emotional you are about it, the more the sympathetic effect to raise cardiac function!
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====Loss of baroreceptor Input====
====Loss of baroreceptor Input====
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*Neck injuries can sever glossopharyngeal nerve, atherosclerosis of the larger arteries can prevent baroreceptors from deforming.
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  Mean arterial pressure normal but wide range of variation each day    Has been duplicated in humans with similar results  1. Seen when aorta and carotid arteries are stiffened with age  2.  Limits cardiovascular responses to body position and     temperature changes 
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*MAP will remain pretty normal, actually, but will have a wider range of variation.
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neural control SAD Dog
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*Even though our average pressure is ok, we have trouble with body position changes.
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**This is orthostatic hypotension; in ability to generate contractility increase and arterial constriction.
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*We also have trouble responding to temperature appropriately.
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*So we must have some long-term system other than baroreceptors to keep our bp over time.
====Loss of all neural control====
====Loss of all neural control====
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    1. Spinal anesthesia or damage      2. Partial recovery from chronic injury associated with increased          sensitivity to norepinephrine 
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*Nerve block in the spine
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Neural control full loss on arterial pressure
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**Useful for having surgery without depressing the brain.
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**This will cause a decrease in bp mostly because peripheral vascular resistance drops
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**Done routinely
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**
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*Pts with spinal cord injuries that inhibit the sympathetics will become supersensitive to NE where they are no longer getting neural stimulation
===The Brain as a Baroreceptor===
===The Brain as a Baroreceptor===
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*The brain is a baroreceptor!
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*All the areas we've talkeda bout in the brian stem will change their firing appropriately if they aren't getting enough oxygen
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====Inadequate perfusion of the brain====
====Inadequate perfusion of the brain====
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  1. Possible causes
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*Let's look at the different scenarios of brain perfusion issues.
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  a.  Arterial pressure too low for autoregulation to be fully protective
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**The theme is inadequate perfusion, oxygen availability decreases, carbon dioxide accumulates, tissue becomes acidotic, sympathetic activity increased dramatically to raise pressure.
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  b. Compromise of the carotid arteries
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  c.  Increased intracranial pressure collapsing first venules then          arterioles  (edema and low perfusion) 
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cerebral baroreceptor flowchart
 
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  2.  Consequences of inadequate perfusion    a.  Oxygen availability decreases in tissue    b.  Carbon dioxide accumulates    c.  Tissue becomes acidotic  B.  Responses:  Sympathetic activity increased dramatically in an        attempt to raise pressure adequately to perfuse the brain       vessels 
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*Arterial pressure too low for autoregulation
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cerebral baroreceptor flowchart
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*Compromise of the carotid arteries
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**Blood flow goes down in brain
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**Sympathetic activity will go up to increase blood pressure so it is high enough to get to the deep part of the brain.
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**If this is caused by arterial disease, it must be very advanced arterial disease such that the patient will have many problems other than getting blood to the brain.
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*Increased intracranial pressure
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**Bump on the head and bleeding into the brain
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**Increased pressure squishes the microvessels and venules, then the arterioles
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**This raises vascular resistance
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**Decreased blood flow
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**Too low oxygen to sympathetics
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**Faster firing of sympathetics
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**Tries to bring blood flow up
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**Cushing reflex:
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***Many pts in early 1900s would die after surgery
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***This happened because of brain swelling after surgery.
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***BP would go really high because of sympathetic response to swelling in the brain
===Long Term Regulation of Arterial Blood Pressure===
===Long Term Regulation of Arterial Blood Pressure===
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*From birth to death, bp on average only changes about 20-30 mmHg!
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*How does the body know to keep bp constant over this long term?
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====Intake of NaCl equals Renal loss of NaCl over a matter of a few days====
====Intake of NaCl equals Renal loss of NaCl over a matter of a few days====
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*There isn't much Na in the natrual environment of humans.
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*NaCl was money in the past
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**Not worth his salt
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*As you consume high levels of salt:
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**Increased NaCl does increase MAP
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**Then body compensates by greater excretion of NaCl to lower blood volume
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*It is generally assumed that the major mean arterial pressure effect of salt is on the central venous pressure and CO.
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What?
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*However, a second effect is the damage done to endothelial cells and vascular smooth muscle cells because of oxygen radical formation.
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*Hypertensive state:
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**Those who have generated a new bp setpoint at a higher level still excrete na and water just fine, it just takes a higher bp for the kidney to be signaled to react.
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    1.  Increased NaCl does increase MAP                      but body compensates by greater                      excretion of NaCl to lower blood volume      2.  Generally assumed that major MAP                            effect of NaCl is blood volume effect                            on central venous pressure and CO.                     
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====If arterial pressure increases and baroreceptors work, less sympathetic nerve activity to kidney allows increased loss of NaCl====
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Increase NaCl Intake
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However, there are negative effects on endothelial and vascular smooth muscle mainly due to increased generation of oxygen radicals   
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====If arterial pressure increases and baroreceptors work, less sympathetic nerve activity to kidney allows       increased loss of NaCl====
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====If intake of NaCl can not be properly excreted, arterial pressure will increase====
====If intake of NaCl can not be properly excreted, arterial pressure will increase====
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*Kidney function goes down with age.
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*BP diseases go up with age, too.
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*So, as one age, because the kidney's can't respond correclty, even if a pt has functional baroreceptors, they may not be able to control BP that is elevated because of NaCl.
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**Eat salt, bp goes up, baroreceptors fire to brain, brain tells kidney to remove Na and water, kidneys try but fail, bp remains high.
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**So we give them a diuretic to increase urination.
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*Na intake is one of the most important long term control mechanisms for blood pressure control.
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*Only one in four pts react to increase or decrease in dietary Na addition or reduction.
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*Black americans are more salt sensitive than most caucasians.
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**Africans have similar sensitivity to cuacasians.
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**What happened?
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***Some people think obesity is over represented in blacks than in africans.
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  Common problem in      many forms of renal disease.  
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====Obesity====
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*Obesity has changed our understanding of hypertension.
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*Obesity affects salt sensitivty, atherosclerotic lipids that affect baroreceptors, leptin production (ncreases sympath and icnreases salt sensitivity).
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*More on this in a couple days.
===Clinical Example===
===Clinical Example===
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*24 yo
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While camping in Florida, a 24 year old medical student went for a vigorous bicycle ride on a very warm day.  When he returned several hours later, he collapsed in his tent. His classmates tried to have him drink water, but he was too unresponsive to swallow properly. At the Emergency Department of a local hospital, the vital signs were as follows:
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*Vigorous activity, heavy sweating
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Heart rate: 127 beats/ min
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*Collapsed in tent, couldn't drink
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Arterial blood pressure:  80/50 mmHg
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*High heart rate; sympathetics are working
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Neck veins and arm veins lying: flattened
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*BP = 80/50
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Facial and body skin : Sweating profusely  
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*Neck veins and arm veins are flat when lying down; his blood volume is really low
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              Vascular refill in fingers: 6 seconds  
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*Facial and body skin : Sweating profusely
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Patient: Unresponsive to name, but both pupils react rapidly to light,   reacts sluggishly to sternal pain stimulus  
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*Vascular refill in fingers: 6 seconds
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**That is super slow!
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What is the primary underlying problem in the student's collapse?
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*Unresponsive to name, but both pupils react rapidly to light, reacts sluggishly to sternal pain stimulus
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**Brain is working, but not enough to make him conscious
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A. Intravascular clotting  
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*A. Intravascular clotting  
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B. Failure of sympathetic nervous system  
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**Not yet, though it will be a problem
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C. Elevated peripheral vascular resistance  
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*B. Failure of sympathetic nervous system  
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D. Inadequate cardiac output  
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**Nope, high heart rate tells us sympt is working
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E. Decreased blood volume  
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*C. Elevated peripheral vascular resistance
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**That's trying to save him to perfuse heart and brain so, no.
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*D. Inadequate cardiac output
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**That is true, but that's not what caused him to go bad
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*E. Decreased blood volume
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**Yes
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*Give saline and some 5% glucose solution
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**Glucose burned off will generate water
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cardiovascular tree Richardson
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*continued on to [[Lecture 8 Shock]] on 01/27/11 at 11:40AM.

Revision as of 15:37, 31 January 2011


Contents

Neural Control

Objectives

  • How do the sympathetic and parasympathetic nervous systems change each of the following: Heart rate, Cardiac Contractility, Arterial Resistance, and venous constriction
  • As the mean arterial pressure is increased, how does the arterial baroreceptor activity (firing rate) change? If the artery containing the baroreceptor sensors could not expand as the pressure is increased, how would baroreceptor activity change?
  • What are atrial and ventricular baroreceptors? During which phases of the heart cycle are they active? When excessively active, what general types of modifications of neural and hormonal control occur?
  • At a conceptual level, there are four centers in the brain stem which interact to regulate the sympathetic and parasympathetic nervous systems. What are the four centers and what major functions does each have?
  • Compare the effects of pleasurable emotions versus fear versus anger on neural control of the cardiovascular system.
  • Complete loss of neural cardiovascular control would result in a very low arterial blood pressure, a heart rate of about 100-110 beats/min (no vagal control), and low cardiac output. Why do these problems occur?
  • How does an increase in the intracranial pressure progressively cause decreased brain blood flow even if the arterial blood pressure is elevated?

Overview of Neural Vascular Regulation

  • Looking at the flow chart.
  • Work through it backward from arterial pressure.

Without regulatory system

  • If we stopped neural control to the cardiovasc system, we would faint.
    • Standing and walking would be very difficult.
    • Mean pressure ~50 mmHg

Range of Activity

  • When sleeping, we use only use 80% of our normal awake function of the neural control.
  • When exercising, CV flow icnreases 5-10 fold, at least.
  • BP and cardiac output goes up because of the symp nervous system

Must adapt to life span of >80 years

  • Most of us will see 2100
  • Our bp will change very little over time if we stay lean and active
  • Even from little babies to full grown, our BP doesn't change much:
    • Increase in about 20-30 mmHg.
    • This occurs as the child starts to stand.

Set Point Pressure

  • Setpoint pressure:
    • The moment at which the body will try to maintain the bp.
    • When sleeping, the pressure is about 80.
    • awake = 90
    • walking and talking = 95
    • Walk fast = 105
    • Run in the hall 140-150.
    • These are each new setpoints
  • Resistance and volume and what not get fixed to maintain these set points.

E. Regulated variables

  • Let's look at at 24 hour cycle: noon to noon with a healthy, normal male
  • Variables that are regulated:
    • Mean arterail pressure, pretty constant:
      • BP drops off with sleep
      • BP goes up with alarm clock
        • BP usually highest in the mornings
    • Heart rate:
      • Low while sleeping
      • High in the morning
    • Stroke volume
      • Boringly constant
      • Except when exercising
      • Can increase 40%
    • Cardiac output
      • Low while sleeping
      • Up during exercise, though not much
      • 50% in increase is a nice walk, not a run or anything
    • Total peripheral resistance
      • Went up during sleep
      • Went down when "busy" in the evening


  • 24 hours with an athlete:
    • Mean arterail pressure, pretty constant:
      • Decreases where it needs to, goes up where the blood isn't needed.
    • Heart rate:
      • Heart rate is lower because cardiac output is higher
      • can go really low, too.
      • Max heart rate isn't really that different as sedentary people; may even be that athletes can't quite as high.
    • Stroke volume
      • Larger in this athlete
    • Cardiac output
      • Higher
    • Total peripheral resistance
      • Low
    • Venous constriction follows directional changes in heart rate
      • Constrict to make sure the blood is in the right places (organs, arteries).
    • Blood Volume:
      • Exercise training increases blood volume, first by increased plasma.
      • Then RBCs are added later.
      • Volume stays up 5-10% for as long as you exercise.
      • Temperature during the seasons change the blood volume:
        • In the summer the plasma is warmer and the volume increases appropriately
        • The blood volume even changes by the night day cycles (higher in the day, lower in the night when it is cooler).


  • stopped here on 01/27/11 at 9AM.
  • started here on 01/27/11 at 11AM.


Short Term Sensor Systems for Neural Regulation

  • This is moment to moment regulation.
  • CV system can respond very quickly.
  • How does it know?

Peripheral Arterial Baroreceptors

  • The first two lines of defense are baroreceptors:
  • Baroreceptors are found in the arch of aorta and the bifurcation area of common carotid arteries in the neck
  • Mixed into wall of vessel
  • Associated with smooth muscle cells
  • As diameter gets larger, the baroreceptors fire
  • They sense tension of themselves too and will fire
  • As BP goes up they fire faster and faster
  • Carotid baroreceptor is
    • innervated by glossopharyngeal nerve
    • It is the main receptor becasue it works over a wider range
  • Aortic arch receptor
    • Vagus
    • Only over pressures over MAP; stops working over 100 mmHg
    • Can signal when the pressure drops under 100 to tell the brain pressure is low
Baroreceptor function
  • How do they work?
  • Mechanosensitive Na and Ca channels
  • Ions rush in
  • More depolarization, the faster the signal to the brain trhough glosso and vagus nerves
Influences on baroreceptor function
  • This firing is influenced by things in our bodies like abnormal lipid levels, normal or abnomral production of prostacyclins and NO, etc.
  • Prostacylins and NO (vasodilators):
    • When smooth muscles relaxed, there is more tenstion on the barorecptors because there is more tension
    • So baroreceptors fire
    • This is good because sympathetics should calm when pressure is going up.
  • When lipids are high:
    • Too much LDLs
    • endothelial cells aren't healthy, don't make NO or prostacyclins
    • So we don't get relaxation of smooth muscle
    • We don't get baroreceptor stretch
    • We don't get sympathetic inhibition
    • Blood pressure rises as sympathetics keep signaling smooth muscle to flex and narrow arteries
  • Platelet activation:
    • Usually act as vasoconstrictyors
    • BAroreceptors are inhibited
    • Parasympathetics are signaled to fire
    • Body thinks blood pressure is going up but it isn't

Low pressure baroreceptors

  • There are baroreceptors in the heart.
    • They can cause increase or decrease of neural stimulation at the heart.
  • Atrial Type A baroreceptors:
    • These monitor atrial contract; tell the brain if it is going well or not.
  • Atrial type B
    • Sense how venous pressure is stretching the atrium.
    • Brain stops getting signal if not stretching correctly.
  • Ventricular receptors
    • These sense how well the ventricle is being passively stretched.
  • Different ventricular receptors
    • Detect tension generated during systole
  • If Atrial type a or b are over active, brain is told that atria are doing too much (too much stretch in diastole, or something)
    • Antidiuretic hormone is suppressed to reduce blood volume.
    • Sympathetic activity will also be suppressed.
  • If too much ventricular activit / stretch is detected:
    • Symnpathetic activity is decreased.
    • These are more important than the atrial baroreceptors.
    • Renal lectures will tell us about how atria can release hormones to talk to the kidneys, too.

Integration of Input and Output Neural Signals in the Medulla Excitatory Centers

  • Higher the bp pressure, more firing of baroreceptors.
  • This is a reciprocal innervation system: the more the baroreceptors fire, the more they inhibit cardiac excitatory systems (in the brain stem).
    • Brain stem is generally where sympathetics originate.

Pressor Center - sympathetic nervous system to blood vessels

  • The pressor center is part of the sympahetics.
  • It talks to the blood vessels
  • When inhibited, less activity to the arteries so they are less constricted.
  • Tries to bring bp up through: venus constriction, arterial constriction, increased heart contractility

Cardiac inhibitory center

  • This is the beginning of the parasympathetics.
  • When these fire, the vagus nerve gets stimulated
  • Vagus goes to SA node, AV node and slows the heart rate
    • Most effective at SA node but also at AV node.
  • Notice that vagus does not (nor does any of the parasymp) affect blood vessels.

Cardiac Excitatory Center - sympathetic nervous system to heart

  • The sympthetic system is tonically active.
    • it must be inhibited or it will fire very fast.
    • Baroreceptors are all calming the parasymp down.


Overall outcome of the baroreceptor and central nervous system interaction

  • As baroreceptor activity is increased, the medulla will reflexively decrease the sympathetic nervous system activity; vagal activity usually changes in the opposite direction of sympathetic activity.
  • The cardiovascular system without sympathetic or parasympathetic activity:
    • Heart rate about 100-110 beats/min,
      • SA node has an inherent rate of about 100, so as we rest, parasympathetics dominate HR control (ach > ne)
    • Arterial pressure 65/40 mmHg,
      • pretty low
    • Cardiac output about 70% of normal,
      • Need sympath NE to generate proper heart contraction
    • Vasculatures very dilated,
      • need sympath NE to keep vessels a little constricted
    • Skin warm,
    • mucus membranes flushed,
    • very little tolerance to sitting or standing
      • Because of low cardiac output
  • The Full Neural Control System:
    • Heart rate should be 70-80 beats / min,
    • arterial pressure 120/70 mmHg,
    • cardiac output 70 ml/min per kg,
    • skin cool and
    • mucus membranes pink,
      • not too much blood flow to the skin
    • able to perform to the maximum ability of the skeletal muscle system.

Modifications of Neural Control By Higher Brain Centers

  • This is the conscious brain working on our unconscious systems.

Emotion

  • Pleasurable sensations
    • BP goes down
    • People who pet dogs or have pets brings down bp.
    • Pleasure lowers sympathetic and increases parasympathetic activity
  • Anger
    • Excites the sympathetics
    • Acts in the brain, increase firing rate of sympathetic neurons
    • Can be so potent as to cause an heart attack
    • Anger also decreases sensitivity of the baroreceptors
  • Fear and depression
    • Inhibits sympathetic activity
    • Works from conscious centers in brain
    • There is a depression of the sympathetics in the medulla
    • There is a stimulation of the parasympathetic system; this can cause fainting because of the slowed heart rate and low vascular resistance.

Pain

  • Sharp pain - activate sympathetic system
    • jazzes up the sympathetics
  • Visceral pain - suppress sympathetic system
    • Childbirth, kidney stone, hit in the chest in car accident

Exercise

  • Just knowing you're going to exercise causes increase in sympathetic activity
  • The more emotional you are about it, the more the sympathetic effect to raise cardiac function!

Loss of baroreceptor Input

  • Neck injuries can sever glossopharyngeal nerve, atherosclerosis of the larger arteries can prevent baroreceptors from deforming.
  • MAP will remain pretty normal, actually, but will have a wider range of variation.
  • Even though our average pressure is ok, we have trouble with body position changes.
    • This is orthostatic hypotension; in ability to generate contractility increase and arterial constriction.
  • We also have trouble responding to temperature appropriately.
  • So we must have some long-term system other than baroreceptors to keep our bp over time.

Loss of all neural control

  • Nerve block in the spine
    • Useful for having surgery without depressing the brain.
    • This will cause a decrease in bp mostly because peripheral vascular resistance drops
    • Done routinely
  • Pts with spinal cord injuries that inhibit the sympathetics will become supersensitive to NE where they are no longer getting neural stimulation

The Brain as a Baroreceptor

  • The brain is a baroreceptor!
  • All the areas we've talkeda bout in the brian stem will change their firing appropriately if they aren't getting enough oxygen

Inadequate perfusion of the brain

  • Let's look at the different scenarios of brain perfusion issues.
    • The theme is inadequate perfusion, oxygen availability decreases, carbon dioxide accumulates, tissue becomes acidotic, sympathetic activity increased dramatically to raise pressure.


  • Arterial pressure too low for autoregulation
  • Compromise of the carotid arteries
    • Blood flow goes down in brain
    • Sympathetic activity will go up to increase blood pressure so it is high enough to get to the deep part of the brain.
    • If this is caused by arterial disease, it must be very advanced arterial disease such that the patient will have many problems other than getting blood to the brain.
  • Increased intracranial pressure
    • Bump on the head and bleeding into the brain
    • Increased pressure squishes the microvessels and venules, then the arterioles
    • This raises vascular resistance
    • Decreased blood flow
    • Too low oxygen to sympathetics
    • Faster firing of sympathetics
    • Tries to bring blood flow up
    • Cushing reflex:
      • Many pts in early 1900s would die after surgery
      • This happened because of brain swelling after surgery.
      • BP would go really high because of sympathetic response to swelling in the brain

Long Term Regulation of Arterial Blood Pressure

  • From birth to death, bp on average only changes about 20-30 mmHg!
  • How does the body know to keep bp constant over this long term?

Intake of NaCl equals Renal loss of NaCl over a matter of a few days

  • There isn't much Na in the natrual environment of humans.
  • NaCl was money in the past
    • Not worth his salt
  • As you consume high levels of salt:
    • Increased NaCl does increase MAP
    • Then body compensates by greater excretion of NaCl to lower blood volume
  • It is generally assumed that the major mean arterial pressure effect of salt is on the central venous pressure and CO. 
What?
  • However, a second effect is the damage done to endothelial cells and vascular smooth muscle cells because of oxygen radical formation.
  • Hypertensive state:
    • Those who have generated a new bp setpoint at a higher level still excrete na and water just fine, it just takes a higher bp for the kidney to be signaled to react.

If arterial pressure increases and baroreceptors work, less sympathetic nerve activity to kidney allows increased loss of NaCl

If intake of NaCl can not be properly excreted, arterial pressure will increase

  • Kidney function goes down with age.
  • BP diseases go up with age, too.
  • So, as one age, because the kidney's can't respond correclty, even if a pt has functional baroreceptors, they may not be able to control BP that is elevated because of NaCl.
    • Eat salt, bp goes up, baroreceptors fire to brain, brain tells kidney to remove Na and water, kidneys try but fail, bp remains high.
    • So we give them a diuretic to increase urination.
  • Na intake is one of the most important long term control mechanisms for blood pressure control.
  • Only one in four pts react to increase or decrease in dietary Na addition or reduction.
  • Black americans are more salt sensitive than most caucasians.
    • Africans have similar sensitivity to cuacasians.
    • What happened?
      • Some people think obesity is over represented in blacks than in africans.

Obesity

  • Obesity has changed our understanding of hypertension.
  • Obesity affects salt sensitivty, atherosclerotic lipids that affect baroreceptors, leptin production (ncreases sympath and icnreases salt sensitivity).
  • More on this in a couple days.

Clinical Example

  • 24 yo
  • Vigorous activity, heavy sweating
  • Collapsed in tent, couldn't drink
  • High heart rate; sympathetics are working
  • BP = 80/50
  • Neck veins and arm veins are flat when lying down; his blood volume is really low
  • Facial and body skin : Sweating profusely
  • Vascular refill in fingers: 6 seconds
    • That is super slow!
  • Unresponsive to name, but both pupils react rapidly to light, reacts sluggishly to sternal pain stimulus
    • Brain is working, but not enough to make him conscious
  • A. Intravascular clotting
    • Not yet, though it will be a problem
  • B. Failure of sympathetic nervous system
    • Nope, high heart rate tells us sympt is working
  • C. Elevated peripheral vascular resistance
    • That's trying to save him to perfuse heart and brain so, no.
  • D. Inadequate cardiac output
    • That is true, but that's not what caused him to go bad
  • E. Decreased blood volume
    • Yes
  • Give saline and some 5% glucose solution
    • Glucose burned off will generate water


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