Carotid sinus and aortic arch stretch receptors adjust autonomic outflow within seconds
Mnemonic
“Stretch means slow”: baroreceptors fire more when the pressure rises, and the reflex response is to bring it down.
- Receptors - carotid sinus (via the glossopharyngeal, IX) and the aortic arch (via the vagus, X)
- Rising pressure increases firing, which increases parasympathetic and decreases sympathetic outflow, causing bradycardia and vasodilatation
- Falling pressure does the reverse, causing tachycardia and vasoconstriction
“Carotid nine, aortic ten” for the afferents.
The reflex is what corrects blood pressure on standing and during haemorrhage, and its failure causes postural hypotension, which is why autonomic neuropathy, ageing and antihypertensives all produce it.
Carotid sinus massage exploits the reflex to slow the heart and unmask atrial activity in a supraventricular tachycardia, and carotid sinus hypersensitivity is a cause of syncope in the elderly.
Baroreceptors reset within days to a new pressure, which is why they do not correct chronic hypertension.
Expansion
- Receptors - stretch receptors in the carotid sinus and aortic arch
- Afferents - carotid via the glossopharyngeal nerve (Hering’s nerve), aortic via the vagus
- Centre - nucleus tractus solitarius in the medulla
- Efferents - vagal and sympathetic outflow
When pressure rises: increased firing inhibits sympathetic outflow and increases vagal tone, producing bradycardia, reduced contractility and vasodilatation, so pressure falls.
When pressure falls: reduced firing removes that inhibition, causing tachycardia, vasoconstriction and venoconstriction.
The reflex acts within seconds and is the mechanism preventing a fall in pressure on standing. It resets over days in sustained hypertension, which is why it does not correct chronic hypertension.
Carotid sinus massage exploits it deliberately to slow atrioventricular conduction, and an oversensitive reflex causes carotid sinus hypersensitivity and syncope.