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.
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.
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.
At a MAP below approximately 50 mm Hg, baroreceptors are completely silent.
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