The baroreflex or baroreceptor reflex is one of the body's homeostatic mechanisms
that helps to maintain blood pressure at nearly constant levels. The baroreflex
provides a rapid negative feedback loop in which an elevated blood pressure
reflexively causes the heart rate to decrease and also causing blood pressure
to decrease. Decreased blood pressure decreases baroreflex activation and
causes heart rate to increase and to restore blood pressure levels. The
baroreflex can begin to act in less than the duration of a cardiac cycle and thus
baroreflex adjustments are key factors in dealing with postural hypotension,
the tendency for blood pressure to decrease on standing due to gravity.
The system relies on specialized neurons, known as baroreceptors, in the
aortic arch, carotid sinuses, and elsewhere to monitor changes in blood
pressure and relay them to the brainstem. Baroreceptors are stretch
receptors and respond to the pressure induced stretching of the blood vessel
in which they are found. Baroreflex induced changes in blood pressure are
mediated by both branches of the autonomic nervous system - that is the
parasympathetic and sympathetic nerves. Baroreceptors are active even at normal
blood pressures so that their activity informs the brain about both increases
and decreases in blood pressure. The body contains two other, slower
acting systems to regulate blood pressure: the heart releases atrial
natriuretic peptide when blood pressure is too high, and the kidneys sense and
correct low blood pressure with the renin-angiotensin system.
Anatomy of the reflex Baroreceptors are present in the
auricles of the heart and vena cavae, but the most sensitive baroreceptors are
in the carotid sinuses and aortic arch. While the carotid sinus baroreceptor
axons travel within the glossopharyngeal nerve, the aortic arch baroreceptor
axons travel within the vagus nerve. Baroreceptor activity travels along
these nerves directly into the central nervous system to contact neurons within
the nucleus of the solitary tract in the brainstem. Baroreceptor information
flows from these NTS neurons to both parasympathetic and sympathetic neurons
within the brainstem. The NTS neurons send excitatory fibers
to the caudal ventrolateral medulla, activating the CVLM. The activated CVLM
then sends inhibitory fibers to the rostral ventrolateral medulla, thus
inhibiting the RVLM. The RVLM is the primary regulator of the sympathetic
nervous system, sending excitatory fibers to the sympathetic preganglionic
neurons located in the intermediolateral nucleus of the spinal cord. Hence, when
the baroreceptors are activated, the NTS activates the CVLM, which in turn
inhibits the RVLM, thus decreasing the activity of the sympathetic branch of
the autonomic nervous system, leading to a relative decrease in blood pressure.
Likewise, low blood pressure activates baroreceptors less and causes an
increase in sympathetic tone via "disinhibition" of the RVLM.
Cardiovascular targets of the sympathetic nervous system includes both
blood vessels and the heart. Even at resting levels of blood
pressure, arterial baroreceptor discharge activates NTS neurons. Some of
these NTS neurons are tonically activated by this resting blood pressure
and thus activate excitatory fibers to the nucleus ambiguus and Dorsal nucleus
of vagus nerve to regulate the parasympathetic nervous system. These
parasympathetic neurons send axons to the heart and parasympathetic activity
slows cardiac pacemaking and thus heart rate. This parasympathetic activity is
further increased during conditions of elevated blood pressure. Note that the
parasympathetic nervous system is primarily directed toward the heart.
Baroreceptor activation The baroreceptors are stretch-sensitive
mechanoreceptors. At low pressures, baroreceptors become inactive. When
blood pressure rises, the carotid and aortic sinuses are distended further,
resulting in increased stretch and, therefore, a greater degree of
activation of the baroreceptors. At normal resting blood pressures, many
baroreceptors are actively reporting blood pressure information and the
baroreflex is actively modulating autonomic activity. Active baroreceptors
fire action potentials more frequently. The greater the stretch the more rapidly
baroreceptors fire action potentials. Many individual baroreceptors are
inactive at normal resting pressures and only become activated when their stretch
or pressure threshold is exceeded. Baroreceptor action potentials are
relayed to the nucleus of the tractus solitarius, which uses frequency as a
measure of blood pressure. As discussed previously, increased activation of the
NTS inhibits the vasomotor center and stimulates the vagal nuclei. The
end-result of baroreceptor activation is inhibition of the sympathetic nervous
system and activation of the parasympathetic nervous system.
The sympathetic and parasympathetic branches of the autonomic nervous system
have opposing effects on blood pressure. Sympathetic activation leads to an
elevation of total peripheral resistance and cardiac output via increased
contractility of the heart, heart rate, and arterial vasoconstriction, which
tends to increase blood pressure. Conversely, parasympathetic activation
leads to decreased cardiac output via decrease in heart rate, resulting in a
tendency to lower blood pressure. By coupling sympathetic inhibition and
parasympathetic activation, the baroreflex maximizes blood pressure
reduction. Sympathetic inhibition leads to a drop in peripheral resistance,
while parasympathetic activation leads to a depressed heart rate and
contractility. The combined effects will dramatically decrease blood pressure.
In a similar manner, sympathetic activation with parasympathetic
inhibition allows the baroreflex to elevate blood pressure.
Set point and tonic activation Baroreceptor firing has an inhibitory
effect on sympathetic outflow. The sympathetic neurons fire at different
rates which determines the release of norepinephrine onto cardiovascular
targets. Norepinephrine constricts blood vessels to increase blood pressure. When
baroreceptors are stretched their firing rate increases which in turn decreases
the sympathetic outflow resulting in reduced norepinephrine and a thus blood
pressure. When the blood pressure is low, baroreceptor firing is reduced and
this in turn results in augmented sympathetic outflow and increased
norepinephrine release on the heart and blood vessels, increasing blood
pressure. Effect on heart rate variability
The baroreflex may be responsible for a part of the low-frequency component of
heart rate variability, the so-called Mayer waves, at 0.1 Hz [Sleight, 1995].
Baroreflex activation therapy for treatment of resistant hypertension
Published feasibility studies have shown that a pacemaker-like device designed to
electrically activate the baroreceptors, also known as baroreflex activation
therapy, significantly lowers blood pressure in patients with
treatment-resistant hypertension. One study published on a group of 16
patients reported an average systolic blood pressure reduction of 34 mmHg
after three months of treatment and 35 mmHg after 24 months. A drop in systolic
blood pressure of at least 20 mmHg was achieved in 12 of 16 patients at 2
years, and 5 of 16 achieved a systolic BP of less than 140 mmHg at 2 years.
Results published on a separate group of 10 patients from another feasibility
trial reported an average systolic blood pressure reduction of 24 mmHg after
three months of treatment. Baroreflex activation therapy devices have received
CE Mark for European sale, but have not received FDA approval for sale in the
United States. See also
Autonomic nervous system Baroreceptor
Blood pressure Heart rate turbulence
Reflex bradycardia Valsalva Maneuver
References Boron, Walter F., Boulpaep, Emile L..
Medical Physiology: A Cellular and Molecular Approach. Philadelphia, PA:
Elsevier/Saunders. ISBN 1-4160-2328-3. Sleight, P.; M.T. La Rovere; A. Mortara;
G. Pinna; R. Maestri; S. Leuzzi; B. Bianchini; L. Tavazzi; L. Bernardi.
"Physiology and pathophysiology of heart rate and blood pressure variability in
humans. Is power spectral analysis largely an index of baroreflex gain?".
Clinical Science, 88: 103–109. Heesch, C.. "Reflexes that control
cardiovascular function". American Journal of Physiology, 277: S234–S243.