Baroreflex
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In cardiovascular physiology, 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 blood pressure to decrease; similarly, decreased blood pressure depresses the baroreflex, causing blood pressure to rise.
The system relies on specialized neurons (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.
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[edit] Anatomy of the reflex
Baroreceptors include those 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 inhibitory fibers to the vasomotor center (VMC), which regulates activity of the sympathetic nervous system, and excitatory fibers to vagal nuclei that regulate the parasympathetic nervous system. Thus, an active NTS inhibits sympathetic outflow and stimulates parasympathetic outflow, while an inactive NTS leads to sympathetic activation and parasympathetic inhibition.
[edit] 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 spike frequency as a surrogate 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 increased contractility of the heart, increased heart rate, venoconstriction, and arterial vasoconstriction, which tend to increase blood pressure by elevating both total peripheral resistance and cardiac output. Conversely, parasympathetic activation leads to a decrease in heart rate and a minor decrease in contractility, resulting in a decreased cardiac output and therefore a tendency to decrease blood pressure.
By coupling sympathetic inhibition with parasympathetic activation, the baroreflex maximizes its ability to reduce blood pressure. Sympathetic inhibition leads to a drop in total peripheral resistance and cardiac output, while parasympathetic activation leads to a depressed heart rate and reduced cardiac contractility. The combined effects will dramatically decrease blood pressure.
Similarly, coupling sympathetic activation with parasympathetic inhibition allows the baroreflex to elevate blood pressure effectively. Sympathetic activation increases total peripheral resistance and elevates cardiac output, the latter being enhanced by inhibition of the parasympathetic nervous system.
[edit] Set point and tonic activation
Baroreceptors are tonically active at mean arterial pressures (MAP) above approximately 70 mm Hg, called the baroreceptor set point. When MAP falls below the set point, baroreceptors are essentially silent. The baroreceptor set point is not fixed; its value may change with changes in blood pressure that persist for 1-2 days. For example, in chronic hypertension, the set point will increase; on the other hand, chronic hypotension will result in a depression of the baroreceptor set point.
At a MAP below approximately 50 mm Hg, baroreceptors are completely silent.
[edit] 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.[citation needed]
[edit] See also
[edit] References
- Berne, Robert M., Levy, Matthew N. (2001). Cardiovascular Physiology. Philadelphia, PA: Mosby.
- Boron, Walter F., Boulpaep, Emile L. (2005). Medical Physiology: A Cellular and Molecular Approach. Philadelphia, PA: Elsevier/Saunders.
