Hubbry Logo
BaroreflexBaroreflexMain
Open search
Baroreflex
Community hub
Baroreflex
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Contribute something
Baroreflex
Baroreflex
Baroreflex
View on Wikipedia
from Wikipedia
Flowchart showing baroreceptor reflex

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

[edit]

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

[edit]

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 mechanosensitivity is hypothesised to be linked to the expression of PIEZO1 and PIEZO2 on neurons in the petrosal 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

[edit]

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

[edit]

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

[edit]
Baroreflex activation is distinct from vagal stimulation. It works through an afferent limb which has the double effect of stimulating vagal outflow and attenuating global sympathetic outflow.

High blood pressure

[edit]

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

[edit]

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

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Baroreflex

View on Grokipedia
from Grokipedia
The baroreflex is a fundamental negative feedback mechanism in the cardiovascular system that maintains arterial blood pressure homeostasis by detecting changes in blood pressure and eliciting rapid autonomic adjustments to heart rate, cardiac output, and vascular tone. This reflex primarily involves baroreceptors, specialized mechanoreceptors located in the walls of the carotid sinus and aortic arch, which sense stretch induced by blood pressure fluctuations and transmit afferent signals via the glossopharyngeal and vagus nerves to the nucleus tractus solitarius in the medulla oblongata. Upon activation, increased baroreceptor firing during hypertension inhibits sympathetic outflow while enhancing parasympathetic activity, leading to bradycardia, reduced contractility, and vasodilation to lower pressure; conversely, hypotension decreases firing, promoting sympathetic activation for tachycardia, increased contractility, and vasoconstriction to raise pressure. Baroreceptors include two main fiber types: rapidly adapting A-fibers that respond to dynamic pressure changes and tonic C-fibers that provide basal control, with additional low-pressure receptors in the cardiopulmonary regions contributing to volume regulation. The baroreflex operates on a beat-to-beat basis for short-term buffering of variability, exhibiting resonance around a 10-second period known as Mayer waves, and plays a in preventing excessive hypotensive or hypertensive excursions during postural changes, exercise, or stress. Baroreflex sensitivity (BRS) quantifies the reflex's efficiency, typically measured as the change in interbeat interval per unit change in systolic (e.g., ms/mmHg), reflecting the balance between parasympathetic and sympathetic influences on the . Beyond acute regulation, the baroreflex contributes to long-term cardiovascular stability by modulating sympathetic nerve activity to the kidneys and vasculature, thereby influencing and peripheral resistance. Its impairment is associated with conditions like and , underscoring its protective role against arrhythmias and excessive sympathetic drive.

Anatomy and Components

Baroreceptors

Baroreceptors are specialized mechanoreceptors embedded in the walls of major arteries that detect fluctuations in by sensing the mechanical stretch of the vascular wall. These sensory structures convert mechanical deformation into electrical signals, providing critical feedback for cardiovascular regulation. Primarily, arterial baroreceptors are located in two key sites: the , at the bifurcation of the common carotid arteries, and the , near the origin of the major arterial branches. The baroreceptors are innervated by the (cranial nerve IX) via the sinus nerve of Hering, while those in the are innervated by the (cranial nerve X) through the aortic depressor nerve. Baroreceptor afferent fibers are categorized into A-type and C-type based on myelination and conduction characteristics. A-type fibers are myelinated, enabling rapid signal transmission and higher maximum firing rates (typically 50-150 Hz in response to acute changes), whereas C-type fibers are unmyelinated, with slower conduction and lower firing rates (typically 2-20 Hz). A-type fibers predominate in phasic responses to rapid variations, while C-type fibers contribute to tonic signaling during sustained levels. Firing activity generally increases above a threshold of approximately 60 mmHg in normotensive adults, with saturation occurring around 180 mmHg, though thresholds can shift with age or pathology. Structurally, baroreceptor endings consist of spray-like, unencapsulated nerve terminals forming intricate branching networks primarily within the adventitia, the outermost layer of the arterial wall, with occasional extensions into the adjacent outer media layer. These endings are particularly dense in elastic regions of the carotid sinus and aortic arch, where the vessel wall is thinner and more compliant to facilitate deformation. Pressure-induced stretch of the wall displaces these terminals, opening stretch-activated ion channels—such as mechanosensitive cation channels—that allow influx of ions like sodium and calcium, leading to membrane depolarization and action potential generation in the afferent fibers. In addition to high-pressure arterial baroreceptors, low-pressure baroreceptors are located in the walls of the great veins, pulmonary vessels, atria, and ventricles. These receptors primarily detect changes in central and low-pressure distension rather than arterial pressure, contributing to the of balance, renal sympathetic activity, and hormone release such as . They are innervated mainly by vagal afferents and project to the nucleus tractus solitarius, integrating with arterial baroreflex pathways for overall cardiovascular . Baroreceptors have evolved as a conserved feature for blood pressure across s, appearing in forms from fish to mammals, where they elicit reflexive adjustments in and vascular tone. Comparative studies reveal a consistent baroreflex response—such as upon receptor loading—throughout vertebrate classes, with increasing sophistication in mammalian systems due to enhanced neural integration and sensitivity. This evolutionary persistence underscores their fundamental role in maintaining circulatory stability against environmental and physiological challenges.

Neural Pathways

The afferent pathway of the baroreflex begins with in the and , which transmit sensory information via the (cranial nerve IX) from the and the (cranial nerve X) from the to the nucleus tractus solitarius (NTS) in the dorsomedial . These unmyelinated and myelinated fibers carry stretch-sensitive signals that encode arterial pressure changes. In the , the NTS serves as the primary integration site, receiving and processing inputs before projecting to downstream regions. Excitatory projections from the NTS target the caudal ventrolateral medulla (CVLM), where inhibit the rostral ventrolateral medulla (RVLM), thereby reducing sympathetic premotor activity and overall sympathetic outflow. The NTS also modulates the RVLM directly and indirectly through other pathways to fine-tune cardiovascular responses. The efferent limb of the baroreflex consists of parasympathetic and sympathetic components that execute the reflex adjustments. Parasympathetic efferents originate from NTS-activated preganglionic neurons in the nucleus ambiguus and dorsal motor nucleus of the vagus, traveling via the vagus nerve to the sinoatrial node to decrease heart rate. Sympathetic efferents, modulated by inhibitory inputs from the CVLM to the RVLM, descend through the spinal cord (primarily intermediolateral cell column at T1-L2 levels) to postganglionic neurons innervating the heart and blood vessels, resulting in reduced vasoconstriction and cardiac output. Key neurotransmitters facilitate signal transmission along these pathways: glutamate acts as the primary excitatory transmitter in baroreceptor afferents to the NTS and in NTS projections to the CVLM and parasympathetic nuclei, while GABA mediates inhibition from CVLM neurons to RVLM neurons, and norepinephrine is released by postganglionic sympathetic fibers to modulate vascular tone and . The baroreflex pathways exhibit bilateral organization with significant redundancy, as and central components on both sides of the contribute to function, minimizing the impact of unilateral damage through crossover projections and compensatory mechanisms from the contralateral side or cardiopulmonary afferents. Consequently, unilateral lesions, such as those affecting the NTS region, typically produce only partial dysfunction rather than complete failure.

Physiological Mechanism

Activation Process

The baroreflex is triggered by an acute rise in , which stretches the walls of the and , activating mechanosensitive embedded in these regions. This mechanical deformation increases the frequency of action potentials in baroreceptor afferent , with firing rates rising linearly as elevates from approximately 60 to 180 mmHg, where sensitivity peaks near normal arterial pressures of 85–100 mmHg. cease firing below threshold pressures around 50–60 mmHg, allowing for rapid detection of hypertensive events. Signal transduction occurs as the stretch of nerve endings opens stretch-activated cation channels, such as TRPC5 or DEG/ENaC family members, permitting influx of ions like sodium and calcium that the afferent nerve terminals. This generates action potentials that propagate via myelinated A-fibers (for dynamic changes) or unmyelinated C-fibers (for sustained input), encoding pressure information through , typically ranging from 0 to 200 Hz depending on the intensity of stretch. The afferents from the travel via the , while those from the use the , converging in the nucleus tractus solitarius (NTS) in the . Central processing in the NTS is rapid, occurring on the order of milliseconds to 150 ms, where baroreceptor inputs inhibit rostral ventrolateral medulla (RVLM) neurons to suppress sympathetic outflow while exciting parasympathetic nuclei to enhance . This timeline enables near-instantaneous autonomic adjustments, with parasympathetic effects manifesting in 200–600 ms. The immediate effectors include , achieved through increased vagal stimulation of the to slow , and peripheral resulting from withdrawal of sympathetic vasoconstrictor activity to reduce . The activation process distinguishes between phasic and tonic components: phasic activation responds to pulsatile pressure variations within each , primarily via A-fibers to buffer beat-to-beat fluctuations, while tonic activation reflects changes, mediated more by C-fibers for steady-state regulation. The overall sensitivity of the baroreflex is often quantified by its gain, expressed mathematically as the change in R-R interval per unit change in : Baroreflex gain=ΔRRIΔBP\text{Baroreflex gain} = \frac{\Delta \text{RRI}}{\Delta \text{BP}} In healthy humans, this typically ranges from -10 to -20 ms/mmHg, indicating a 10–20 ms prolongation of the R-R interval for each 1 mmHg rise in pressure, underscoring the reflex's role in acute pressure stabilization.

Set Point and Tonic Regulation

The baroreflex set point represents the central nervous system's preset reference value for mean arterial pressure (MAP), around which the reflex operates to maintain cardiovascular homeostasis, typically ranging from 85 to 100 mmHg in healthy adults. This operating point ensures that small deviations in pressure elicit proportional changes in baroreceptor firing rates, thereby stabilizing blood pressure through negative feedback. At rest, the baroreflex operates via tonic activation, characterized by continuous low-level firing of arterial baroreceptors that provides a baseline inhibitory influence on sympathetic nervous system outflow while facilitating parasympathetic tone to the heart and vessels. This steady-state balance prevents excessive fluctuations in heart rate and vascular resistance, allowing the cardiovascular system to function efficiently without constant acute adjustments. The set point is not fixed and can undergo short-term resetting over hours in response to physiological demands, such as elevated angiotensin II levels or dynamic exercise, which shift the upward to support higher without compromising sensitivity. For instance, during exercise, the baroreflex resets to a higher threshold, enabling increased and while preserving the 's gain. In conditions like acute induced by angiotensin II, this resetting occurs within 48 hours and contributes to sustained elevations in by altering the central integration of signals. Several factors modulate the baroreflex set point and its tonic regulation. Aging progressively reduces baroreflex sensitivity, shifting the set point and diminishing the reflex's ability to buffer pressure changes effectively. During , particularly rapid eye movement () stages, sympathetic activation increases, lowering baroreflex sensitivity and adjusting the set point downward compared to non-REM sleep or wakefulness. Postural changes, such as assuming an upright position, trigger orthostatic adjustments that transiently reset the set point upward to counteract gravitational effects on venous return and maintain cerebral . The baroreflex also demonstrates , where the threshold pressure for activation differs depending on whether is rising or falling, due to mechanical and in . This property ensures asymmetric responses that favor rapid correction of over , enhancing stability during pressure transitions. In terms of tonic control, the steady-state aligns with the set point in equilibrium, as persistent error signals from deviations are integrated over time by central mechanisms to minimize long-term offsets, akin to a proportional-integral feedback model.

Functional Effects

Cardiovascular Responses

The baroreflex modulates heart rate primarily through reciprocal adjustments in parasympathetic and sympathetic nervous system activity to the sinoatrial node. During hypotension, reduced baroreceptor firing leads to parasympathetic withdrawal and sympathetic activation, resulting in tachycardia that helps restore blood pressure by increasing cardiac output. Conversely, in response to hypertension, heightened baroreceptor discharge enhances parasympathetic dominance (vagal tone) and inhibits sympathetic outflow, producing bradycardia via reversal of sinoatrial node inhibition. Vascular tone is regulated by the baroreflex through alterations in sympathetic efferents to arterioles and veins. An elevation in triggers baroreflex-mediated inhibition of sympathetic activity, withdrawing vasoconstrictor tone and promoting , which reduces total peripheral resistance and aids in lowering pressure. In , increased sympathetic drive enhances , elevating peripheral resistance to support . These vascular adjustments complement changes to achieve rapid . Cardiac output is influenced by baroreflex effects on both and . Hypertension elicits decreased sympathetic stimulation to the ventricles, reducing inotropic support and alongside , thereby lowering overall . During , sympathetic enhancement boosts contractility and , increasing to counteract the pressure drop. The integrated baroreflex response buffers acute perturbations, such as those occurring during postural shifts from to standing, where it mitigates excessive through coordinated increases in and . The baroreflex interacts with other reflexes, where it can be overridden or reset under specific conditions. For instance, the chemoreflex during hypoxia may suppress baroreflex to permit necessary elevations for oxygen delivery, while the exercise pressor response—driven by central command and group III/IV muscle afferents—resets the baroreflex operating point to higher pressures, allowing and vascular tone to rise despite inputs that might otherwise oppose such changes. Quantitatively, in young adults, a 10 mmHg rise in typically elicits a decrease of approximately 10 bpm, reflecting robust baroreflex gain under resting conditions.

Impact on Heart Rate Variability

The baroreflex plays a key role in modulating high-frequency components of heart rate variability (HRV), particularly in the range of 0.15-0.4 Hz, through its interaction with respiratory sinus arrhythmia (RSA). RSA reflects cyclic fluctuations in heart rate synchronized with breathing, primarily driven by parasympathetic activity, but the baroreflex contributes by adjusting vagal outflow in response to respiratory-induced blood pressure changes. This modulation arises from the mechanism by which pulsatile waves, generated by each heartbeat, entrain firing patterns, leading to cyclic variations in parasympathetic tone that influence beat-to-beat intervals. in the and detect these pressure pulses and signal via afferent nerves to the nucleus tractus solitarius, prompting adjustments that enhance parasympathetic inhibition during and allow sympathetic facilitation during , thereby contributing to the rhythmic components of HRV. In spectral analysis of HRV, the baroreflex sensitivity (BRS) strongly correlates with low-frequency HRV power in the 0.04-0.15 Hz band, which largely reflects baroreflex-mediated autonomic regulation rather than pure sympathetic activity. BRS quantifies this relationship and is calculated as the magnitude of the change in RR interval (or heart period) per unit change in systolic : BRS=∣ΔRRΔSBP∣(ms/mmHg)\text{BRS} = \left| \frac{\Delta \text{RR}}{\Delta \text{SBP}} \right| \quad (\text{ms/mmHg})
Add your contribution
Related Hubs
Contribute something
User Avatar
No comments yet.