Baroreflex

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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(頸內(nèi)動脈處), 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 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.[2]

Contents

·?1Anatomy

·?2Activation

·?3Set point and tonic activation

·?4Effect on heart rate variability

·?5Baroreflex activation therapy

·?5.1High blood pressure

·?5.2Heart failure

·?6See also

·?7References

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?nucleus of the solitary tract?(NTS) in the brainstem.[3]Baroreceptor information flows from these NTS neurons to both parasympathetic and sympathetic neurons within the brainstem.[citation needed]

The NTS 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 NTS neurons. Some of these NTS neurons are tonically activated by this resting blood pressure and thus activate excitatory fibers to the nucleus ambiguous 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.[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 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]