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Baroreflex

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The baroreflex or baroreceptor reflex is one of the body's homeostatic mechanisms for maintaining blood pressure. It provides a negative feedback loop in which an elevated blood pressure reflexively causes heart rate to decrease and also causing blood pressure to decrease; likewise, decreased blood pressure activates the baroreflex, causing heart rate to increase, and also causing an increase in blood pressure.

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. Subsequent changes in blood pressure are mediated by the autonomic nervous system. Atrial natriuretic peptide forms a parallel negative feedback loop in an endocrinological contrast to 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. The carotid sinus baroreceptors are innervated by the glossopharyngeal nerve (CN IX); the aortic arch baroreceptors are innervated by the vagus nerve (CN X). Baroreceptor activity travels along these nerves, which contact the nucleus of the solitary tract (NTS) in the brainstem.

The NTS sends excitatory fibers (glutamatergic) to the caudal ventrolateral medulla (CVLM), activating the CVLM. The activated CVLM then sends inhibitory fibers (GABAergic) up 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 inhibiting the sympathetic branch of the autonomic nervous system, leading to a decrease in blood pressure. Likewise, low blood pressure causes an increase in sympathetic tone via "disinhibition" (less inhibition, hence activation) of the RVLM.

The NTS also sends excitatory fibers to the Dorsal nucleus of vagus nerve that regulate the parasympathetic nervous system, aiding in the decrease in sympathetic activity during conditions of elevated blood pressure.

Baroreceptor activation

The baroreceptors are stretch-sensitive mechanoreceptors. When blood pressure rises, the carotid and aortic sinuses are distended, resulting in stretch and, therefore, activation of the baroreceptors. Active baroreceptors fire action potentials ("spikes") more frequently than inactive baroreceptors. The greater the stretch the more rapidly baroreceptors fire action potentials.

These action potentials are relayed to the nucleus of the tractus solitarius (NTS), 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 (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.

Set point and tonic activation

Baroreceptor firing has an inhibitory effect on sympathetic outflow. The sympathetic neurones fire at different rates, releasing various amounts of Norepinephrine. 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 increases the inhibitory effect on sympathetic outflow resulting in reduced norepinephrine production and a corresponding reduction in blood pressure. When the blood pressure is low, baroreceptor firing is lowered; this reduces the inhibitory effect on the sympathetic outflow and consequently an increased amount of norepinephrine is released to receptors, causing blood vessels to constrict thus 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 baroreflex, 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 (75%) patients at 2 years, and 5 of 16 (31%) achieved a systolic BP of less than 140 mmHg at 2 years.[1] 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.[2] 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

References

  1. ^ Scheffers. Journal of Hypertension 2008;26(Suppl 1):S19.
  2. ^ Bisognano J. The Journal of Clinical Hypertension 2006; Suppl A8 (No 4):A43
  • Berne, Robert M., Levy, Matthew N. (2001). Cardiovascular Physiology. Philadelphia, PA: Mosby. ISBN 0-323-01127-6.{{cite book}}: CS1 maint: multiple names: authors list (link)
  • Boron, Walter F., Boulpaep, Emile L. (2005). Medical Physiology: A Cellular and Molecular Approach. Philadelphia, PA: Elsevier/Saunders. ISBN 1-4160-2328-3.{{cite book}}: CS1 maint: multiple names: authors list (link)
  • Sleight, P. (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: 103–109. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: extra punctuation (link)
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