When the baroreceptor reflex is stimulated by a decrease in blood pressure,

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Baroreceptors are a type of mechanoreceptor allowing for the relay of information derived from blood pressure within the autonomic nervous system.

• They are spray-type nerve endings in the walls of blood vessels and the heart that are stimulated by the absolute level of, and changes in, arterial pressure. They are extremely abundant in the wall of the bifurcation of the internal carotid arteries (carotid sinus) and in the wall of the aortic arch[1].

The primary site of termination of baroreceptor afferent fibers is the nucleus tractus solitarius (NTS).  The NTS has been described by many as the primary visceral sensory relay station within the brain. It receives and responds to stimuli from the respiratory, cardiovascular, and gastrointestinal systems[2].

Information is then passed in rapid sequence to alter the total peripheral resistance and cardiac output maintaining blood pressure within a preset, normalized range.

There are two types of baroreceptors:

1. High-pressure arterial baroreceptors and low-pressure volume receptors which are both stimulated by stretching of the vessel wall. Arterial baroreceptors are located within the carotid sinuses and the aortic arch.
2. Low-pressure volume receptors, or cardiopulmonary receptors, are located within the atria, ventricles, and pulmonary vasculature[3]

Function[edit | edit source]

The function of the baroreceptors is to maintain systemic blood pressure at a relatively constant level, especially during a change in body position.

High Pressure Baroreceptors

Intact baroreceptors are extremely effective in preventing rapid changes in blood pressure from moment to moment or hour to hour, but because of their adaptability to prolonged changes of blood pressure (> 2 or 3 days), the system is incapable of long-term regulation of arterial pressure.

• Stretching of the baroreceptors as a result of increased blood pressure causes an increase in the activity of the vagal nerve by projection to the nucleus ambiguus. It also causes inhibition of the sympathetic outflow and ultimately leads to decreased heart rate and blood pressure.
• Conversely, decreased blood pressure results in decreased signal output from the baroreceptors, leading to disinhibition of the central sympathetic control sites and decreased parasympathetic activity. The final effect is an increase in blood pressure.[1]

Low pressure Baroreceptors

These are found in the large veins and in the walls of the atria of the heart. The low pressure baroreceptors are involved with the regulation of blood volume. The blood volume determines the mean pressure throughout the system, in particular in the venous side where most of the blood is held.

The low pressure baroreceptors have both circulatory and renal effects, they produce changes in hormone secretion which have profound effects on the retention of salt and water and also influence intake of salt and water. The renal effects allow the receptors to change the mean pressure in the system in the long term[4].

• Denervating these receptors fools the body into thinking that we have too low blood volume and initiates mechanisms which retain fluid and so push up the blood pressure to a higher level than we would otherwise have.

Pathophysiology[edit | edit source]

Baroreceptors respond very quickly to maintain a stable blood pressure, but they only respond to short term changes. Over a period of days or weeks they will reset to a new value. In people with essential hypertension the baroreceptors behave as if the elevated blood pressure is normal and aim to maintain this high blood pressure.

• Considering new approaches to treating hypertension is crucial. High blood pressure is a very common and important cause of disease and death resulting from problems with the heart, and with the blood vessels in the body and brain. Treatment to lower high blood pressure is supposed to continue for decades. However, even by 12 months after the starting treatment, around 50% of patients are not taking their tablets regularly, if at all[5].

• Carotid pacemakers, Image at R, also known as implantable carotid sinus stimulators, are devices that deliver activation energy, via carotid leads, to the carotid baroreceptors. This is sometimes offered for drug-resistant hypertension. The baroreceptors send signals to the brain and the signals are interpreted as a rise in blood pressure. The brain sends signals to other parts of the body to reduce blood pressure such as the blood vessels, heart and kidneys[6].

On the opposite end of the spectrum, carotid sinus syndrome is a syndrome in which the carotid sinus is particularly sensitive to external pressure. Increased pressure on the carotid sinus, such as from a particularly tight collar or sustained turn of the head, results in significant hypotension and possibly syncope[3].

References[edit | edit source]

Homeostatic mechanism in the body

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 causes the heart rate to decrease. Decreased blood pressure decreases baroreflex activation and causes heart rate to increase and to restore blood pressure levels. Their function is to sense pressure changes by responding to change in the tension of the arterial wall[1] The baroreflex can begin to act in less than the duration of a cardiac cycle (fractions of a second) 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, chiefly in the aortic arch and carotid sinuses, to monitor changes in blood pressure and relay them to the medulla oblongata. 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: the parasympathetic and sympathetic nerves. Baroreceptors are active even at normal blood pressures so 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.[2]

Anatomy

Baroreceptors are present in the atria 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 (CN IX), the aortic arch baroreceptor axons travel within the vagus nerve (CN X). Baroreceptor activity travels along these nerves directly into the central nervous system to excite glutamatergic neurons within the solitary nucleus (SN) in the brainstem.[3] Baroreceptor information flows from these NSS neurons to both parasympathetic and sympathetic neurons within the brainstem.[citation needed]

The SN neurons send excitatory fibers ([[glutamatergic) to the caudal ventrolateral medulla (CVLM), activating the CVLM. The activated CVLM then sends inhibitory fibers (GABAergic) to the rostral ventrolateral medulla (RVLM), thus inhibiting the RVLM. The RVLM is the primary regulator of the sympathetic nervous system, sending excitatory fibers (glutamatergic) to the sympathetic preganglionic neurons located in the intermediolateral nucleus of the spinal cord. Hence, when the baroreceptors are activated (by an increased blood pressure), 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" (less inhibition, hence activation) of the RVLM. Cardiovascular targets of the sympathetic nervous system includes both blood vessels and the heart.[citation needed]

Even at resting levels of blood pressure, arterial baroreceptor discharge activates SN neurons. Some of these SN 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. The parasympathetic nervous system is primarily directed toward the heart.[citation needed]

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 ("spikes") 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.[citation needed]

Baroreceptor mechanosensitivty is hypothesised to be linked to the expression of PIEZO1 and PIEZO2 on neurons in the pretrosal and nodose ganglia.

Baroreceptor action potentials are relayed to the solitary nucleus, which uses frequency as a measure of blood pressure. Increased activation of the solitary nucleus 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.[citation needed]

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.[citation needed]

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 (reflex bradycardia) 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.[citation needed]

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 (due to an increased blood pressure) their firing rate increases which in turn decreases the sympathetic outflow resulting in reduced norepinephrine and 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.[citation needed]

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.[4]

Baroreflex activation therapy

High blood pressure

The baroreflex can be used to treat resistant hypertension.[5] This stimulation is provided by a pacemaker-like device. While the devices appears to lower blood pressure, evidence remains very limited as of 2018.[5]

Heart failure

The ability of baroreflex activation therapy to reduce sympathetic nerve activity suggests a potential in the treatment of chronic heart failure, because in this condition there is often intense sympathetic activation and patients with such sympathetic activation show a markedly increased risk of fatal arrhythmias and death.[citation needed]

One trial[6] has already shown that baroreflex activation therapy improves functional status, quality of life, exercise capacity and N-terminal pro-brain natriuretic peptide.[citation needed]

See also

• Heart rate turbulence
• Valsalva maneuver

References

1. ^ Bär, Karl-Jürgen (2015-06-24). "Cardiac Autonomic Dysfunction in Patients with Schizophrenia and Their Healthy Relatives – A Small Review". Frontiers in Neurology. Frontiers Media SA. 6: 139. doi:10.3389/fneur.2015.00139. ISSN 1664-2295. PMC 4478389. PMID 26157417.
2. ^ Fu, Shihui; Ping, Ping; Wang, Fengqi; Luo, Leiming (2018-01-12). "Synthesis, secretion, function, metabolism and application of natriuretic peptides in heart failure". Journal of Biological Engineering. Springer Nature. 12 (1): 2. doi:10.1186/s13036-017-0093-0. ISSN 1754-1611. PMC 5766980. PMID 29344085. They are mainly produced by cardiovascular, brain and renal tissues in response to wall stretch and other causes. NPs provide natriuresis, diuresis, vasodilation, antiproliferation, antihypertrophy, antifibrosis and other cardiometabolic protection. NPs represent body’s own antihypertensive system, and provide compensatory protection to counterbalance vasoconstrictor-mitogenic-sodium retaining hormones, released by renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS).
3. ^ Yuan, Jason; Brooks, Heddwen L.; Barman, Susan M.; Barrett, Kim E. (2019). Ganong's Review of Medical Physiology. ISBN 978-1-26-012240-4.
4. ^ Sleight, Peter; La Rovere, Maria Teresa; Mortara, Andrea; Pinna, Gianni; Maestri, Roberto; Leuzzi, Stefano; Bianchini, Beatrice; Tavazzi, Luigi; Bernardi, Luciano (1 January 1995). "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 (1): 103–109. doi:10.1042/cs0880103. PMID 7677832.
5. ^ a b Wallbach, M; Koziolek, MJ (9 November 2017). "Baroreceptors in the carotid and hypertension-systematic review and meta-analysis of the effects of baroreflex activation therapy on blood pressure". Nephrology, Dialysis, Transplantation. 33 (9): 1485–1493. doi:10.1093/ndt/gfx279. PMID 29136223.
6. ^ Abraham, WT; Zile, MR; Weaver, FA; Butter, C; Ducharme, A; Halbach, M; Klug, D; Lovett, EG; Müller-Ehmsen, J; Schafer, JE; Senni, M; Swarup, V; Wachter, R; Little, WC (June 2015). "Baroreflex Activation Therapy for the Treatment of Heart Failure With a Reduced Ejection Fraction". JACC: Heart Failure. 3 (6): 487–496. doi:10.1016/j.jchf.2015.02.006. PMID 25982108.

• Boron, Walter F.; Boulpaep, Emile L. (2005). 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 (1995). "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 (1): 103–109. doi:10.1042/cs0880103. PMID 7677832.
• Heesch, C. (1999). "Reflexes that control cardiovascular function". American Journal of Physiology. 277 (6 Pt 2): S234–S243. doi:10.1152/advances.1999.277.6.S234. PMID 10644250.

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