Objectives have been taken from The American Physiological Society Medical Curriculum Objectives Project

http//:www.the-aps.org/education/MedPhysObj/medcor.htm
In some case, the order of the topics and the objectives have been modify

Objectives:

1. List the anatomical components of the baroreceptor reflex.

2. Explain the sequence of events in the baroreceptor that occur after an acute increase or decrease in
arterial blood pressure. Include receptor response, afferent nerve activity, CNS integration, efferent
nerve activity to SA node, ventricles, arterioles, venules , and hypothalamus.

3. Contrast the sympathetic and parasympathetic nervous system control of the heart rate, contractility,
TPR, and venous capacitance. Predict the cardiovascular consequence of altering sympathetic nerve
activity and parasympathetic nerve activity

4. Outline the cardiovascular reflexes initiated by decreases in blood O2 and increases in blood CO2.

5. CNS ischemic response. Explain the importance and sequence of events of the CNS ischemic
response and the Cushing reaction.

6. Cardiopulmonary receptors. Explain the sequence of events mediated by cardiopulmonary (volume)

receptors that occur after an acute increase or decrease in arterial blood pressure. Include receptor
response, afferent nerve activity, CNS integration efferent nerve activity to the heart, kidney,
hypothalamus, and vasculature.

7. Describe the release, cardiovascular target organs, and mechanisms of cardiovascular effects for
Angiotensin, ANF, EDRF.

8. Kidney in long term regulation of BP. Explain the role of the kidney in the long term regulation of
arterial pressure.

9. Contrast the relative contribution of short-and long term mechanisms in blood pressure and blood
volume regulation

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CENTRAL REGULATORY RESPONSE OF THE HEART AND THE VASCULATURE

Introduction

The cardiovascular system is organized to respond to multiple demands simultaneously, and specially to
meet crises.
Intrinsic mechanism within tissue stabilize tissue flow and capillary pressure within organs. At the same
time, extrinsic mechanism operating via nerves and hormones coordinate functional needs of the
organism as a whole. For example, fear causes neurally mediated constriction of most vascular beds.
Generalized vasoconstriction mobilizes blood from fight-or-flight, while is the heart and striated muscle,
intrinsic mechanism can override the vasoconstrictor signals to allow the muscles to do the work of
escaping.
In time of crisis the vascular function of all organs will be sacrificed to maintain the cerebral blood flow and
to permit the animal or person to escape.

I. REGULATORY CENTERS

A. Vasomotor or vasoconstrictor center - the pressor area-

• Is the major integrative area for all central nervous system control
• Regulates cardiac function with both the sympathetic and parasympathetic nervous outflow.
• Located in the dorsal medulla
• Stimulation causes: cardioacceleration, vasoconstriction, increased myocardial contractility
• Generates continuous low level of neural ctivity in the sympathetic fibers which causes
vasoconstriction (sympathetic tone)
• Tonic activity is modulated by a wide variety of inputs from chemoreceptor and baroreceptors
throughout the body

B. Vasomotor center –the depressor area--

• Located in the ventromedial and caudal region of the medulla

• Caused dilation mediated by the action through vasomotor center and through spinal pathways

C. Hypothalamus

• Integrative center for various regulatory processes such a s

temperature control
• Stimulation of the anterior hypothalamus causes decreased blood
pressure, vasodilation, and bradycardia
• Stimulation of the posterolateral hypothalamus causes tachycardia
and vasocostriction
• Cutaneous thermal receptors induce vasodilation or vasoconstriction
in response to heat and cold respectively

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II. Blood pressure control system

Overall aim of the system is to keep aortic pressure constant and let the organs regulate their own flow
through autoregulation.

A. Blood pressure control is based on negative feedback that requires:

• A detector (sensor receptor)

• Afferent neural pathway
• An integrator or coordinating center
• An efferent neural pathway and
• An effector

B. Integrator or coordinating center

• Pressure information from the peripheral baroreceptors is integrated in the medulla of the
brainstem. The first synapse for all afferent signals is in the Nucleus tractus solitarius (NTS)

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 • Activity in the NTS activates neurons in the dorsal motor nucleus of the vagus (DMV). That in turn
Activates parasympathetic vagal efferent fibers to the heart.
• Activity in the NTS also activates neurons in the nucleus ambiguous. That also activates vagal
efferent fibers to the heart.
• Activity in the NTS also inhibits neurons in the C1 region of the vasomotor area. The outflow from
this area is sympathetic innervation to the peripheral blood vessels, the heart and the adrenal
medulla.

III. The short term control mechanism of blood pressure (neural) are:

1. Baroreceptor reflexes
2. Chemoreceptor reflexes
3. CNS ischemic response (reflex)
4. Cushing reaction
5. Atrial and pulmonary artery reflexes (low pressure receptors)
Atrial reflex to kidney
Bain-bridge reflex

1. Baroreceptor reflexes

Peripheral baroreceptors (stretch receptors) detect a change in the blood pressure. They send their
signals to the medulla which compares the actual pressure to an internal set point. The medulla then
sends information over the autonomic nerves to stimulate or inhibit the blood vessels and heart as is
required. That in turn returns the blood pressure to the set point.

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A. Sensor: Arterial baroreceptors

Location: carotid sinus and arch of aorta

Stimulus: stretch of the vessel

B. Afferent pathway

1. Stretch receptors in the walls of the carotid sinuses. These receptors are innervated by the Herring’s
nerve (branch of the glossopharyngeal.

a. Increased blood pressure stretches the walls and increases their frequency of action potentials. A
fall in pressure decreases the frequency.

b. Are rate-sensitive and respond to pulsatile pressures better than a steady pressure particularly at low
mean pressures

2. The aortic arch has similar receptors that are innervated by the aortic nerve, a branch of the vagus.

3. The Aortic baroreceptors stop firing at pressures below 100 mmHg while carotid sinus receptors
continue firing all the way down to 50 mmHg. Both saturate at about 200 mmHg Then carotid
baroreceptors are more sensitive than aortic

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4. The baroreceptors are sensitive to both mean (MAP) and pulse pressure (PP)
The figure to the right shows the nerve discharge along the glossopharyngeal nerve to the medulla.

The baroreflex acts primarily to control minute-to-minute blood Pressure (pressure changes). The
baroreceptors quickly adapt to long-term changes in pressure.

C. Effectors

1. Heart
2. Blood vessels

D. Efferent Pathway

1. Sympathetic nervous system acts to increase pressure by increasing heart rate, contractility and
constricting the arteries and veins

2. Parasympathetic nervous system acts to decrease pressure by slowing heart rate. Acetylcholine acts to
inhibit cAMP in the heart and lowers contractility. The human ventricle receive very few vagal fibers as a
result the parasympathetic causes only a very light decrease in contractility.
In order to decrease contractility the CNS can do it only by a decrease sympathetic tone.
PS do not have effect on the vasculature.

A reduction in MAP or PP causes constriction of both arterioles and venules. Measurements are made
while manipulating the MAP and PP. The nerve fires with each rise in the arterial pressure. Also the
number of spikes with each pulse increases as the MAP increases.

E. Function of baroreceptors in body posture changes.

When a person stand up after having been lying down, the arterial pressure in the upper parts of the body
tends to drop and sometimes the patient has loss of consciousness. This because of gravity effect that
pulls down blood This drop in pressure immediately causes a decrease in baroreceptors activity and an

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then a strong sympathetic activity to vessels and heart to return to normal the blood pressure in the upper
part of the body.
F. Clamping of both carotid arteries

In a dog, the clamping of both common carotid

arteries (after cutting the two vagus nerves),
causes a drop in sinus pressure, then
baroreceptors are inactivated and the VMC
increase its activity causing the sympathetic
stimulation to the heart and vessels and blood
pressure will remain elevated during the time the
carotid occlusion is maintained. When the
occlusion is release the aortic pressure falls
below the normal as overcompensation and then
return to normal.

G. Blood pressure increases with exercise.

With exercise the working muscles increases the blood flow by active hyperemia, the peripheral
resistances drop and thus the blood pressure. Baroreceptors detect the drop in BP and initiate a reflex to
return pressure back toward the set point pressure but not pass it. In heavy exercise, however, pressure
will actually be higher than before the start of the exercise. That is because the CNS actually increases
the set point during heavy exercise.

2. Peripheral chemoreceptors (carotid and aortic bodies). This is an important mechanism for
maintaining arterial blood pO2, pCO2, and pH within appropriate physiological ranges.

Carotid and aortic bodies are stimulated by:

1. Low PO2 (hypoxemia)
2. High PCO2 (hypercapnia)
3. Low pH

A. Stimulation of the chemoreceptors directly decreases heart rate and constricts the peripheral blood
vessels.

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Generally systemic hypoxia causes a tachycardia due to the increased respiratory activity . The overall
effect is to raise the blood pressure.

B. Circulatory shock and respiratory failure (conditions that decrease arterial pO2 and pH, and increase
PaCO2) dramatically increase chemoreceptor activity leading to enhanced sympathetic outflow to the
heart and vessels via activation of the vasomotor center.

C. The threshold pO2 for activation is about 80 mmHg (normal arterial pO2 is about 95 mmHg). Any
elevation of pCO2 above a normal value of 40 mmHg, or a decrease in pH below 7.4 causes receptor
firing.

If respiratory activity is not allowed to change during chemoreceptor stimulation (thus removing the
influence of lung mechanoreceptors), then chemoreceptor activation causes bradycardia and coronary
vasodilation (both via vagal activation) and systemic vasoconstriction (via sympathetic activation). If
respiratory activity increases, then sympathetic activity stimulates both the heart and vasculature to
increase arterial pressure.

3. Ischemic response of the CNS.

A. Is an emergency control system. Cerebral ischemia at the level of the VMC causes the neurons of the
VMC strongly become activated, this produces a drastic increase in MAP to maximal possible level
(sometimes 250 mmHg). The extreme excitation of the VMC neurons is caused probably by increased
local concentration of CO2 as consequence of the low blood flow what elicit a strong and powerful
sympathetic stimulation to the vasomotor nervous control areas in the brain.

B. The ischemic response of the CNS becomes activated when the MAP falls down 60 mmHg. Reaching
the greatest stimulation with MAP of 15 to 20 mmHg.

4. Cushing reaction

A. Special type of CNS ischemic response is activated by an increase in intra cranial pressure that can
occur from increase in CSF pressure, edema of the brain or an intercranial bleed. The increased pressure
collapses the blood vessels within the vault . The ischemia in the CNS causes intense stimulation of both
the sympathetic and parasympathetic outflow. Because the sympathetic system has the more profound
effect on blood pressure, blood pressure becomes quite high in an attempt to restore the blood flow into
the brain. Because theacetylcholine can inhibit norepinephrine’s effect at the SA node the heart rate will
tends to decrease. Thus the patient will present with a bradycardia and a hypertension.

5. Cardiopulmonary mechanoreceptors

Low pressure receptors (A and B type) are located in the left atrium. A fibers are stimulated by atrial
systole while B fibers are stimulated by atrial distention (increase in volume).

Atrial stretch activates B fibers which:

1. Increases the heart rate (Bainbridge reflex) through a neural reflex. Atrial stretch also increases the rate
by
a direct mechanical effect on the SA node. The Bainbridge reflex is about 50% direct and 50% neural
effect. The overall effect is to detect buildup of blood behind the heart and move it forward.
2. Decreases sympathetic tone to the kidney causing increased filtration and urine formation.
3. Decreased production of vasopressin (anti-diuretic hormone) to promote fluid loss at the kidney.
4. Atrial stretch directly causes production of atrial naturetic peptide (ANP) by the atrial cells. This causes
dilation of blood vessels and loss of sodium and water by the kidney.

The overall effect (2-4 above) is to cause reduced blood volume when the atria are distended and to
decrease MAP.

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IV. Long term regulation of arterial blood pressure. –The kidney-

A. The kidney is the primary controller of long

term arterial blood pressure. Arterial pressure
directly determines fluid loss at the kidney and
thus the kidney controls blood pressure by a
negative feedback system. Salt (and therefore
fluid volume) loss at the kidney is highly
dependent on blood pressure and relatively
independent of salt intake.

B. Renin-Angiotensin system

While some of the kidney’s control is direct

through the effect of arterial pressure on
glomerular filtration, the majority is indirect
through the Rennin-Angiotensin system.

Low blood flow to the kidney causes secretion

of Renin. Renin causes the conversion of
Angiotensinogen in the blood to Angiotensin I.
This is quickly cleaved by ACE in the lungs to
the powerful vasoconstrictor Angiotensin II
(AII).

Besides the action of AII as powerful

constrictor of the peripheral vessels it also
causes the kidney to retain fluid and thus
th
Guyton Hall. Medical Physiology 11 Ed.

increase blood volume.

People with essential hypertension have an elevated set point for fluid loss. Those that are salt-sensitive
also have a decreased slope in the renal function curve. The baroreceptor reflex will quickly adapt (within
3 days) if the kidney’s set point is raised

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