Anatomy, Head and Neck: Carotid Baroreceptors

Structure and Function

Peripheral baroreceptors are located in the aortic arch and carotid sinus. Baroreceptors within the carotid sinus reside at the bifurcation of the common carotid arteries and transmit afferent signals via the glossopharyngeal nerve to the solitary nucleus of the medulla.[3][4]

Stretch-sensitive fibers within the carotid sinus generate afferent signals based on the degree of vascular distension. Increases in arterial pressure result in greater stretch of these fibers, which enhances baroreceptor signaling. The nucleus solitarius, located in the dorsolateral medulla oblongata, serves as the central integration site for afferent input from carotid baroreceptors and initiates reflex responses to maintain hemodynamic stability.[5][6]

The vagus and glossopharyngeal nerves transmit afferent signals to the solitary nucleus of the medulla. In response, efferent signals are sent to the periphery, resulting in venous and arterial vasodilatation to lower blood pressure. This effect occurs through decreased sympathetic outflow, which reduces vasoconstriction and total peripheral resistance.

Parasympathetic efferent signaling to the sinoatrial node increases, reducing heart rate. Simultaneously, reduced sympathetic outflow decreases cardiac contractility and further lowers heart rate, leading to diminished cardiac output. Elevated blood pressure also prompts the kidneys to reduce salt and water retention, contributing to blood pressure reduction.

Efferent responses targeting the heart, vasculature, and kidneys serve as compensatory mechanisms in response to increased blood pressure. Baroreceptor signaling returns to baseline once homeostatic arterial pressure is restored.[7]

In contrast, hemorrhage causes a decline in arterial pressure. This decrease reduces afferent signaling from carotid baroreceptors to the nucleus solitarius via the glossopharyngeal nerve. The resulting efferent response includes increased sympathetic outflow, promoting vasoconstriction, enhanced cardiac contractility, and elevated heart rate. These effects reflect reduced parasympathetic efferent activity. Decreased blood pressure also stimulates renal retention of salt and water, which increases intravascular volume and supports blood pressure restoration. Efferent signals to the heart, vasculature, and kidneys serve as compensatory mechanisms in response to hypotension.[8]

Embryology

Baroreceptors are active during development. Neurotrophic interactions, potentially involving brain-derived neurotrophic factor (BDNF), may support the enhancement of synaptic plasticity within the baroreflex pathway. These sensory neurons originate from the neural crest, which is derived from the ectodermal sheet.

Clinical Significance

Baroreceptors in the aortic arch and carotid sinus play clinically important roles. Increased pressure on the carotid artery, such as during carotid massage, enhances stretch receptor activation and augments afferent baroreceptor signaling. The carotid sinus detects this heightened activity and transmits signals via the glossopharyngeal nerve, which the central nervous system interprets as elevated arterial pressure.

Compensatory efferent signaling through the nucleus solitarius induces venous and arterial dilation, decreases heart rate, prolongs the atrioventricular node refractory period, and reduces systemic blood pressure. This abrupt decline in perfusion pressure can lead to syncope, particularly in individuals with a history of syncope triggered by activities such as shaving or buttoning a shirt, which increase pressure on the carotid artery.[9]

In contrast, carotid occlusion eliminates blood flow to the carotid sinus. Reduced perfusion of the carotid artery diminishes stretch fiber activation, leading to decreased baroreceptor firing. The carotid sinus transmits this reduced afferent signaling via the glossopharyngeal nerve, which the central nervous system misinterprets as hypotension.

Compensatory efferent output from the nucleus solitarius promotes venous and arterial vasoconstriction, elevates heart rate, and increases systemic blood pressure. Carotid occlusive disease, such as carotid stenosis, may present with ischemic stroke due to impaired cerebral perfusion.[10]

The Cushing reaction represents another clinically relevant manifestation of baroreceptor-mediated regulation. This reflex is characterized by a triad of bradycardia, hypertension, and respiratory depression. In this context, elevated intracranial pressure compresses cerebral arterioles, causing ischemia. Resulting increases in arterial partial pressure of carbon dioxide and reductions in pH trigger sympathetic activation to elevate perfusion pressure through systemic hypertension. The associated rise in arterial pressure enhances peripheral baroreceptor stretch and afferent firing. Increased baroreceptor activity initiates a compensatory reflex bradycardia, completing the Cushing reflex triad.[11]