Lecture 44
Nervous Regulation
of
Circulation
By
Dr. Khaled Ibrahim Khalil
By the end of this session, the student should be able to:
o Describe the physiological anatomy of autonomic supply to the
heart and blood vessels.
o Discuss the nervous control of circulatory functions especially
heart rate.
o Describe the role of vasomotor center in regulation of circulatory
functions.
o Describe the various factors affecting activity of vasomotor
center.
 Guyton & Hall Textbook of Physiology - 12th ed. P. 201204.
Sympathetic
Parasympathetic
Anatomy
Origin:
CAC in medulla oblongata
Relay:
In the upper 3 cervical In terminal ganglia In the
Parts supplied:
CIC in the medulla oblogata
ganglia
heart.
The whole heart
All the heart except the
ventricles
Autonomic Receptor
Cardiac muscle
β1 adrenergic receptors
Muscarinic (M2) receptors
Coronary vessels
β2 & α1 adrenergic receptors
Muscarinic (M3) receptors
Functions
Rhythmicity:
↑H.R.
↓H.R.
a) of atria
↑(may initiate extrasystoles)
↓(may stop an attack of P.T)
b) of ventricles
↑(may initiate extrasystoles)
no effect
Excitability:
Conductivity:
↑due to ↓A-V nodal delay ---->
↓P-R interval in ECG.
↓due to ↑A-V nodal delay. So,
it may produce various degrees of
heart block.
Contractility
a) of atria
Increased
Decreased
b) of ventricles
Increased
No effect
Metabolism
Increased
Decreased
O2 consumption
increased
Decreased
Coronary blood flow
increased (see later)
Decreased (see later)
I- Nervous Regulation of HR
The cardiac centers (CIC & CAC) controlling the heart rate are influenced by
impulses from other nerve centers in the brain and by afferent impulses from the body.
A- Impulses from higher centers:
1- The cerebral cortex:
It is the highest center affecting HR directly or indirectly through the
hypothalamus (as in emotions) in the following conditions:
a- Conditioned reflex:
- It is the change in HR in the response to visual, smell, hearing
stimuli or even thinking about something.
- HR may ↑ or ↓ according to the nature of the stimulus.
- These stimuli stimulate certain areas in the frontal lobe of the
cerebral cortex.
- Conditioned reflex is not a true reflex, e.g. if a source of light is
shown to a dog and then the dog's skin is pricked, the painful
stimulus leads to marked ↑ in HR. With repetition of the
experiment application of light alone without painful stimulus ----> marked ↑ HR.
b- Voluntarily:
Some people can ↑ or ↓ HR voluntarily as in practitioner of yoga.
c- Emotions:
- Most emotions (mild) e.g. fear, anger, sexual excitation…etc -----> ↑ HR.
- Sudden shocking news (sever) ------> ↓ HR.
2- The hypothalamus:
The hypothalamus is the higher center of the autonomic nervous system.
a-
Stimulation of anterior hypothalamic nuclei, which control parasympathetic
activities -----> ↓ HR due to stimulation of CIC. This occurs in quite sleep and in
sever emotion.
b- Stimulation of posterior hypothalamic nuclei, which control sympathetic activities
-----> ↑ HR due to stimulation of CAC. This occurs in mild emotion, stress,
muscular exercise or anxiety as just before starting a race or examination.
3- The respiratory center:
- HR ↑ with inspiration & ↓ with expiration.
- This regular alternation in HR with the respiratory movement is called the
"respiratory sinus arrhythmia".
- It is commonly seen in young individuals.
- Mechanism: ↑ HR during inspiration is due to:
a- Central mechanism:
The active inspiratory center irradiates causing stimulation of the CAC.
b- Peripheral mechanism:
* Lung inflation stimulates the stretch receptors in the alveoli ----> afferent impulses via
the pulmonary vagi -----> -- CIC and ++ CAC.
* Harrison's reflex: see later.
During expiration, HR ↓ due to decreased activity of inspiratory
center, elastic recoil of the lungs and decreased venous return.
B- Afferent impulses affecting the medullary cardiac centers:
1- Afferent impulses from the circulatory system:
It is the most important impulses that regulate HR as it represents (-ve
feedback mechanism) by which several circulatory functions are regulated as
arterial blood pressure & circulatory volume.
Impulses from the right side of the
heart
Bainbridge reflex
McDowal's reflex
Impulses from the left side of
the heart
Marey's law
Bainbridge reflex:
-Increased cardiac filling i.e. right atrial pressure, leads to reflex acceleration of
the heart.
Stimulus: ↑ right atrial pressure (RAP) as in ↑ed venous return or infusion of
blood or saline.
Receptors: atrial baroreceptorsThey are volume mechanoreceptors present in the
wall of right atrium at its junction with superior vena cava & inferior vena cava.
Afferent: vagal fibers.
Center: - - CIC & ++ CAC.
Efferent: Sympathetic fibers.
Response: ++ SAN -----> ↑ HR.
- Significance:
↑ HR ------> ↑ COP
This helps pumping of excess venous return to the arterial side and prevents
stagnation of blood in veins i.e. (diastasis).
McDowal's reflex:
Decreased venous return, i.e., decreased right atrial pressure as in hemorrhage leads
to reflex increase of heart rate and of vasoconstrictor tone of arterioles and venules.
Significance:
This helps to maintain the normal arterial blood pressure to allow sufficient
supply of blood flow to the vital organs as the brain, heart, and kidneys.
Marey's law
The heart rate is inversely proportional to the arterial blood pressure provided
that
other
factors
that
affect
the
heart
rate
remain
constant.
i.e., ↑ ABP -----> ↓ HR & vice versa
Stimulus: ↑ arterial blood pressure (ABP).
Receptors: arterial baroreceptors.In the wall of carotid sinus & aortic arch.
Afferent: sinus nerve (branch of IX) & aortic nerve (branch of X). They are
called "depressor nerves" because they resist rise in ABP.
Center: + + CIC & - - CAC.
Efferent: vagus nerve.
Response: - - SAN -----> ↓ HR.
Significance:↓ ed HR antagonizes the elevation of ABP & helps to restore it to
its normal level.
The “Buffer” function of the baroreceptors control system:
Because the baroreceptor system opposes increases and decreases in arterial
pressure, it is often called a pressure buffer system, and the nerves from the
baroreceptors are called buffer nerves.
Carotid sinus syndrome
Definition:
This is a pathological condition in which the carotid sinus is abnormally
hypersensitive.
Manifestations:
In patients with this syndrome, a slight pressure on the carotid sinus (e.g. during
shaving or by tight collar) stimulates the baroreceptors in the carotid sinus
----> reflex ↑ vagal tone to the heart & ↓ sympathetic vasoconstrictor tone to
the blood vessels -----> bradycardia (↓ HR) and hypotension (↓ ABP) ------>
cerebral ischemia and momentarily loss of consciousness (fainting).
Treatment:
Denervation of the hypersensitive carotid sinus cure the condition.
Clinical significance:
Carotid sinus reflex could be used to terminate an attack of paroxysmal
atrial tachycardia but not of ventricular origin, as the vagus does not
supply the ventricles.
2- Afferent impulses form the body other than the circulatory system:
Stimulation of the central end of any nerve containing afferent fibers e.g. radial,
sciatic or splanchnic may produce ↑ or ↓ HR according to the nature of the
stimulus.
a- Impulses from skeletal muscles (Alams Smirk reflex):
Contraction of voluntary muscles produces reflex increase in heart rate.
- This occurs even with moving one finger.
- Mechanism: Muscle contraction -----> + + proprioceptors in the muscle and
joints ----> afferent somatic sensory nerves -----> + + CAC & - - CIC ----> ↑
HR.
- Significance: help to ↑ blood supply to the active muscle.
- It is a reflex, so, it is obtained after obstruction of the blood supply, and this proves that
it is not due to the metabolites of muscular contraction acting on the cardiac centers or
directly on the SAN.
b- Impulses from pain receptors:
- Mild pain sensation (cutaneous) -----> reflex tachycardia, due to ++ CAC & - - CIC.
- However, sever pain (visceral) -----> reflex bradycardia.
c- Trigger zone reflexes:
The carotid sinus, the eye ball, the larynx, the epigastrium and testes are
sensitive areas known as trigger zones. A blow on any of these areas can produce reflex
severe bradycardia, fainting or even cardiac arrest.
THE VASOMOTOR CENTER (VMC)
Vasomotor center is formed of:
1- Vasoconstrictor center.
2- Vasodilator center.
The vasoconstrictor center (VCC):
- located bilaterally in the antrolateral
portion of the upper medulla.
- It is also called vasopressor area.
- Course:
Neurons of VCC project descending
axons -----> LHCs of all thorathic &
upper 3 lumbar (spinal or subsidiary
VCC) -----> preganglionic to relay in
sympathetic chain or collateral ganglia -----> postganglionic noradrenergic fibers
in spinal nerves -----> SMF of blood
vessels -----> VC of blood vessels.
Mechanism of activity of the VMC:
Under normal resting conditions the VMC is exposed to:
Pressor effect of normal
CO2 tension in the blood
causing stimulation of the
VMC.
Depressor effect of arterial
baroreceptors in the aortic
arch and carotid sinus by the
normal level of ABP causing
inhibition of the VMC.
Normally, the stimulatory effect of CO2 predominates,
leading to continuous discharge from the VCC, producing the VC
tone.
Vasomotor Tone:
Definition: Continuous partial V.C. of arteries & arterioles at rest.
Mechanism: Contineous partial activity of VCC (see before).
Significance: maintain peripheral resistance & Diastolic ABP.
Spinal subsidiary vasomotor centers:
- The bilateral horn cells of the thoracolumbar region of the spinal
cord
- When they are separated from the VCC, they stop transmission of
the VC impulses leading to VD and marked drop of arterial blood
pressure.
b. The vasodilator center (VDC):
- It is located bilaterally in the antrolateral portion of the lower half
of the medulla.
- The fibers from these neurons project upward to the
vasoconstrictor center
- When it is stimulated it inhibits the vasoconstrictor activity of the
VCC, thus causing vasodilatation.
- There is no direct connection between the VDC and the vasodilator
nerves.
Factors affecting the vasomotor center
These factors can be classified into nervous and chemical factors
I. Nervous factors:
1. Impulses from the higher centers:
a. The cerebral cortex:
- can either stimulate or inhibit the VMC depending on the site, and
the intensity of the stimulus.
b. The hypothalamus:
- Stimulation of the postrolateral portions of the hypothalamus ----->
excitation ------> V.C. & ↑ABP.
-Stimulation of the anterior part ------> inhibition --------> VD & 
ABP.
- Moderate emotion ------> ++ VMC ------> VC --------> ↑ABP,
while severe emotion ----> -- VMC ------> ↓ ABP.
- Muscular exercise ++ VMC -----> ↑ABP.
c. The respiratory center:
- The active respiratory center can stimulate the VMC directly by
radiation
- ABP increases during the late part of inspiration and early part of
expiration, while it decreases during the late part of expiration and
early part of inspiration
2. Afferent impulses from the circulatory system:
a. From the arterial
baroreceptors:
Stimulation
aortic
of
the
arch
carotid
and
sinus
receptors
increased
by
level
of
ABP, send depressor
impulses
vasomotor
to
the
center,
producing VD and
drop at ABP.
b.
From
the
chemoreceptors:
Stimulated by O2
lack, CO2 excess or
increased
H+
concentration
in
the blood. When
stimulated
they
send
pressor
impulses to the
VMC,
causing
vasoconstriction
with
consequent
rise of ABP.
c. From the atrial
baroreceptors:
A fall of the right
atrial pressure e.g.
during hemorrhage,
sends
pressor
impulses to the VMC.
Stimulation of the
VMC
leads
to
arteriolar constriction,
which
result
in
elevation of ABP
towards normal level.
3. Afferent impulses from other parts of the body:
1) Cutaneous pain: mild ------> ++ VMC , sever ------> -- VMC
2) Sever visceral pain or afferent fibers from the trigger zones -VMC.
3) Afferent impulses from the Propiroceptors of skeletal muscles
during exercise ++ VMC.
4) Loven's reflex:
Stimulation of the afferent nerve of an organ produces local
vasodilatation in the active organ but generalized vasoconstriction
due to stimulation of the VMC.
5) Cold pressor test:
If a normal person drips his hand in a cold water (4oC), ABP rises by
10-20 mmHg, due to stimulation of the VMC
II. Chemical factors:
1. CO2 tension in the blood: ↑
2. O2 tension in the blood:
3. H+ in the blood ↑
Stimulate VMC