Thanks for your question on the baroreceptor reflex pathway.
To start, here is a good website that explains the pathway, complete
with a diagram showing the connections:
The primary baroreceptors are located in the carotid arteries (the
carotid sinuses) in the neck and sense blood pressure. Pressing on
both baroreceptors at the same time (do NOT try this) will result in
the system perceiving a very high systemic blood pressure and will
signal a drop in blood pressure by decreasing heart rate and cardiac
stroke volume. In a normal person, this will result in the person
fainting (syncope) and can cause cardiac arrest, stroke, or death.
More detail on the other sensors can be found at the webpage above,
including the afferent pathways (which Cranial Nerves carry the
signal), if you desire more information.
To summarize the pathway, high or low blood pressure is sensed in one
of the sensors, which are sensitive to stretching of the blood vessel
in which they are located. Sensors can be found in the carotid
sinuses and the aortic arch. Signals are sent to the central nervous
system (CNS) via Cranial Nerves IX and X respectively.
In the CNS, this information is processed and integrated the Nucleus
Tractus Solitarius located in the brainstem (specifically the medulla
oblongata, the lower portion of the brain that deals with breathing,
cardiac function, etc.). The perceived blood pressure is compared
with a "set point" desired blood pressure, and the appropriate action
Blood pressure is adjusted by the CNS sending nervous signals to
various effectors in the heart, arteries, and veins. Signals to the
sinoatrial (SA) node via the parasympathetic pathways in the Vagus
nerve (Cranial Nerve X) slow down the heart for high pressure,
decreased signal to the Vagus allows the heart to speed up. The
natural, disconnected rate of the heart is fairly high - there is a
constant "tone" in the Vagus that keeps the heart at a "normal" rate.
This tone is increased or decreased in part by the mechanism just
Another diagram of these pathways can be found here, in Figure 1:
Pressure is also adjusted by signals sent to the heart muscle by the
medulla outside of the Vagus pathway. For a high pressure, this
results in lower stroke volume and vice versa. The overall effect of
the changes in stroke volume and heart rate is a change in cardiac
output. These are related through the formula
CO = SV x HR
Blood pressure is directly related to cardiac output, so changing
either the stroke volume or the heart rate effects the blood pressure.
Signals are also sent to the arteries and veins from the medulla,
causing them to constrict or relax if the pressure is perceived as too
low or too high respectively.
The system functions moment-to-moment, but the "set point" can change
over time. In a sense, the baroreceptor system is a mechanism for
enacting the set point in the brain, but doesn't determine the set
point. In people with essential hypertension, it is believed that the
(elevated) pressure sensed by the baroreceptors is perceived as normal
and the system, after a long period of time, functions to maintain
this elevated blood pressure. Also, the system attempts to compensate
for changes in blood pressure, but is not always able to do so. For
example, in severe shock, the blood pressure falls in spite of a
person being tachycardic because the tachycardia isn't enough to
compensate for the decrease in volume or decrease in vascular tone.
There are also low pressure baroreceptors in large veins and in the
atria of the heart. More information on these, as well as on
baroreceptors in general at the Wikipedia page here:
If the nerves from the arterial baroreceptors (branches of Cranial
Nerves IX and X) were cut, signals from these receptors would not
reach the medulla, and only the venous (low pressure) baroreceptor
signals from the atrium and large veins would reach the brain. These
venous baroreceptors effect the kidneys and veins and change the
long-term blood pressure via hormonal signals.
The result of denervation of this type is hemodynamic instability.
One can actually see this type of instability after carotid artery
angioplasty if the carotid sinus is injured. Here is a page from
Medscape describing such a scenario:
Here is an excerpt:
"Iatrogenic injury to the afferent limb of the baroreflex such as that
encountered during CEA [Carotid Endarterrectomy] or CA [Carotid
Artery] angioplasty and stent placement can lead to a reduced
sensitivity of the reflex, thereby causing the patient to experience
lability of the BP. Full-blown baroreflex failure rarely occurs after
these procedures and leads to uninhibited sympathetic discharge,
causing patients to experience diaphoresis and labile hypertension
from excessive catecholamine release, similar to what is seen in
patients with pheochromocytoma. Labile hypertension has been linked to
intracerebral hemorrhage after CEA. With both CEA and CA angioplasty
and stent placement, many reports have been published showing that
patients can experience postoperative hypotension (common with both
procedures) or hypertension (more common with CEA)."
Essentially, there is uninhibited sympathetic signaling, which
increases heart rate and stroke volume (and therefore cardiac output),
similar to what is seen in patients with pheochromocytoma (a tumor of
the adrenal glands that causes excessive secretion of catecholamines
such as epinephrine and norepinephrine). Here is more information:
Another paper from The Netherlands looked at carotid baroreceptor
denervation in humans:
"Carotid baroreceptor denervation in humans causes a persistent
decrease in vagal and sympathetic baroreflex sensitivity and an
increase in blood pressure variability; however, carotid denervation
does not lead to chronic hypertension. Therefore, although carotid
baroreceptors contribute to short-term blood pressure control, other
receptors are able to maintain normal chronic blood pressure levels in
the absence of carotid baroreceptors."
You can find the full text of the article here:
This article also has a good discussion of the baroreceptor reflex.
Although not really your question, another interesting situation to
consider is the effect of all of this on a transplanted (completely
denervated) heart. These hearts respond to humoral signals, but not
sympathetic or parasympathetic signals. More information can be found
"The pathophysiology of the transplanted heart is unique. The
denervation of the organ makes it dependent on its intrinsic rate. As
a result of the lack of neuronal input, some left ventricular
hypertrophy results. The right-sided function is directly dependent
upon the ischemic time incurred prior to reimplantation and the
adequacy of preservation. The right ventricle is easily damaged and
may initially function as a passive conduit until recovery occurs."
You may also benefit from the following article about hypersensitivity
of the carotid baroreceptors (Weiss-Baker Syndrome), which can result
in dizziness and fainting (syncope):
I hope this information was helpful. Please feel free to request any