Baroreceptor reflex
Also known as: baroreflex, carotid sinus reflex, Bainbridge reflex, Cushing reflex
The baroreceptor reflex is a fast negative-feedback loop that buffers moment-to-moment changes in arterial pressure. Stretch receptors in the carotid sinus and aortic arch signal to the medulla, which adjusts heart rate, contractility and vascular tone within seconds.
Overview
Afferent limb. Stretch-sensitive nerve endings in the carotid sinus send signals through the carotid sinus nerve, a branch of CN IX. Those in the aortic arch signal through the vagus nerve (CN X). Both pathways end in the nucleus tractus solitarius (NTS) in the medulla. The receptors fire faster as the arterial wall stretches, and they respond to how quickly pressure is changing as well as to its level. The carotid sinus works over roughly 60–180 mmHg and is most sensitive near normal MAP.
Response to a rise in pressure. When blood pressure rises, baroreceptor firing increases. The NTS then does two things. First, it excites the vagal motor neurons in the nucleus ambiguus and dorsal motor nucleus, which slows the heart. Second, through inhibitory neurons in the caudal ventrolateral medulla, it inhibits the sympathetic output from the rostral ventrolateral medulla (RVLM). With less sympathetic drive, heart rate and contractility fall, arterioles dilate and veins relax. Cardiac output and total peripheral resistance therefore fall, and blood pressure returns toward normal. A fall in pressure produces the opposite response.
Resetting. Within one to two days, baroreceptors adapt to a sustained new pressure. This is why they correct short-term changes, such as on standing up, but do not set the long-term level of blood pressure.
Parts & subdivisions
- In the carotid sinus (signalling through CN IX) and the aortic arch (signalling through CN X).
- Cardiopulmonary (low-pressure) receptorsIn the atria, great veins and pulmonary vessels. When stretched by a large blood volume, they reduce ADH release and renal sympathetic activity and increase ANP release. Atrial stretch can also raise heart rate (the Bainbridge reflex).
- Chemoreceptor reflexThe carotid and aortic bodies respond to low PO₂, high PCO₂ and high H⁺. When MAP falls below about 80 mmHg, they also drive strong sympathetic vasoconstriction.
- CNS ischaemic response (Cushing reflex)When intracranial pressure is very high, brainstem ischaemia triggers a massive rise in sympathetic activity. The result is the Cushing triad: hypertension, a reflex slowing of the heart and irregular breathing.
Function
- Buffers short-term fluctuations in arterial pressure, for example on changes of posture, exercise or straining.
- Maintains brain perfusion when standing up.
Clinical significance
Postural adaptation and orthostatic hypotension
On standing, about 500–700 mL of blood pools in the legs. Within seconds the baroreflex raises heart rate and peripheral resistance to keep blood pressure up. If this reflex fails, as in autonomic neuropathy, Parkinson disease or with some drugs, orthostatic hypotension and fainting result.
Valsalva manoeuvre and vagal manoeuvres
Forced expiration against a closed glottis (the Valsalva manoeuvre) causes a characteristic four-phase change in blood pressure and heart rate, which can be used to test the baroreflex. Vagal manoeuvres, such as the modified Valsalva or carotid sinus massage, can stop AV nodal re-entrant tachycardia.
Vasovagal syncope
In vasovagal syncope, a trigger such as prolonged standing, pain or emotion causes a sudden drop in sympathetic activity and a surge in vagal activity. The heart slows and the blood vessels dilate, so blood pressure falls and the person faints.
Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.