Introduction

Baroreceptors are a type of mechanoreceptors allowing for relaying information derived from blood pressure within the autonomic nervous system. Information is then passed in rapid sequence to alter the total peripheral resistance and cardiac output, maintaining blood pressure within a preset, normalized range. There are two types of baroreceptors: high-pressure arterial baroreceptors and low-pressure volume receptors, which are both stimulated by stretching of the vessel wall. Arterial baroreceptors are located within the carotid sinuses and the aortic arch. Low-pressure volume receptors, or cardiopulmonary receptors, are located within the atria, ventricles, and pulmonary vasculature.[1]

Cellular Level

The conduction system of the baroreceptors divides into two groups. Large, myelinated A-fibers are responsible for the dynamic changes for second to second monitoring and maintenance of blood pressure and heart rate, which is accomplished by myelinated fibers having more rapid transmission via jumping of synapses for the continuation of action potentials. Smaller, unmyelinated type C-fibers offer a tonic, basal control of blood pressure and heart rate. Should the blood pressure drop, the aortic baroreceptor firing rate will decrease due to less arterial wall strain. The decreased firing rate will propagate to the nucleus tractus solitarius, and changes to the body’s vascular resistance, heart rate, and cardiac contractility will occur.[2][3]

Development

Carotid bodies develop from a conglomeration of neural crest cells, nerve fibers, and blood vessels after sympathetic and cranial nerve ganglia invade the wall of the third branchial arch’s mesenchymal primordia.[4]

Organ Systems Involved

Carotid Sinus Nerve

The carotid sinus nerve (CSN) originates from the glossopharyngeal nerve near the exit from the jugular foramen. Impulses sent via the carotid sinus transmit along the CSN to the glossopharyngeal nerve, which synapses with the nucleus tractus solitarius (NTS) in the medulla. The CSN demonstrates multiple communication sites with the sympathetic trunk (frequently at the level of the superior cervical ganglion) and vagal trunk (often near the main trunk, superior laryngeal nerve, and pharyngeal branches). The course of the CSN is predominantly on the anterior aspect of the internal carotid artery to reach the carotid sinus, carotid body, and intercarotid plexus.[5]

Carotid Sinus and Carotid Body

The carotid sinus has two types of fibers for transmission of vasculature status. Type 1 carotid baroreceptors, also known as dynamic baroreceptors, have large, myelinated A-fibers. Type 2 baroreceptors, also known as tonic baroreceptors, have small A-fibers and unmyelinated C-fibers. Simulation by acetylcholine and ATP result in the transmission of information through the afferent fibers of the carotid body.

Arterial Baroreceptors

Impulses sent via the carotid sinus transmit along the carotid sinus nerve to the glossopharyngeal nerve, which synapses with the NTS in the medulla. Impulses originating in the aortic arch travel along afferent fibers of the vagus nerve to synapse at the NTS. The NTS tonically provides sympathetic outflow to peripheral vasculature. Stimulation of the NTS results in inhibition of sympathetic tone and a vasodilatory effect with associated decreased cardiac output.[6]

Cardiopulmonary Receptors

Impulses transmit from the atria to the vagal center of the medulla via the vagal nerve. As a result, sympathetic outflow to the kidney is reduced, resulting in decreased renal blood flow and decreased urine output. Alternatively, the sympathetic outflow is increased to the sinus node in the atria resulting in increased heart rate and, therefore, cardiac output. Additionally, vagal stimulation inhibits the vasoconstrictor center of the medulla resulting in decreased release of angiotensin, aldosterone, and vasopressin.

There are two types of cardiopulmonary receptors within the atria. Type A receptors are activated by wall tension developed by atrial contraction during ventricular diastole, while type B receptors are activated by wall stretch developed by atrial filling during ventricular systole.[7]

Function

Arterial baroreceptors function to inform the autonomic nervous system of beat-to-beat changes in blood pressure within the arterial system. Rapid decreases in blood pressure, such as in orthostatic hypotension, resulted in decreased stretching of the artery wall and decreased action potential frequency, ultimately resulting in increased cardiac output and vasoconstriction resulting in increased blood pressure. The opposite is found to be true of increased blood pressure.

Cardiopulmonary receptors, or volume receptors, are similarly mechanoreceptors that function to inform the autonomic nervous system of the blood volume within the system. In low volume states, circulatory and renal changes result in increased salt and water resorption within the kidneys, increased salt and water oral intake, and slower, longer-term mean pressure changes.[8]

One study showed that the carotid baroreceptor reflex could regulate cerebral blood flow at rest and during dynamic exercise. This study was small, with only seven subjects around the age of 26. It found that with heavy exercise, middle cerebral artery blood flow tripled, and cerebral tissue oxygenation was almost tripled, but prazosin was able to blunt the mean arterial pressure, cerebral oxygenation, and cerebral blood flow during exercise and at rest. Prazosin is a sympatholytic medication and an alpha-1 blocker resulting in vascular smooth muscle relaxation. The choice of this drug was due to the vascular smooth musculature found in the carotid sinus, carotid body, and cerebral vasculature.

Another small study with only 8 participants found that group III/IV afferent muscle fibers are critical in resetting the carotid baroreflex mean arterial pressure and heart rate operating points despite changes induced by exercise when a subject is in command of the spontaneous movements.[9]

Cardiopulmonary receptors have strong associations with body position changes and with activation evoke sympathoinhibition demonstrated by a small study of 13 healthy men around the age of 21 showing an increase in heart rate, stroke volume, and cardiac output when subjects are in seated positions as opposed to no changes while in the supine position. These changes are blunted to statistical insignificance with a beta-1 adrenergic blockade, such as with atenolol, demonstrating the sympathetic mediation of cardiac responses.

Mechanism

Baroreceptor exerts control of mean arterial pressure as a negative feedback loop. Nerve impulses from arterial baroreceptors are tonically active; increases in arterial blood pressure will result in an increased rate of impulse firing. Increased stimulation of the nucleus tractus solitarius by arterial baroreceptors results in increased inhibition of the tonically active sympathetic outflow to peripheral vasculature, resulting in vasodilation and decreased peripheral vascular resistance. The opposite is true of decreases in mean arterial pressure, resulting in decreased nerve firing and reduced stimulation of the nucleus tractus solitarius, thereby attenuating inhibition and increasing sympathetic outflow to peripheral vasculature and vasoconstriction.

Similarly, nerve impulses from cardiopulmonary baroreceptors are also tonically active and increase their rate of firing secondary to increased blood volume and mean arterial pressure results in decreased sympathetic outflow to the sinoatrial node and decreased heart rate and cardiac output. In a notable difference, sympathetic outflow to the kidney increases, which increases renal blood flow and urine production, thereby decreasing the fluid volume of the body.[10]

Pathophysiology

Baroreceptor resetting has been implicated in the maintenance of inappropriately elevated mean arterial pressures, while on the opposite end of the spectrum, carotid sinus syndrome is a syndrome in which the carotid sinus is particularly sensitive to external pressure. Increased pressure on the carotid sinus, such as from a particularly tight collar or sustained turn of the head, results in significant hypotension and possibly syncope.[11][12]

Clinical Significance

Carotid sinus sensitivity can result in syncope with stimulation of the carotid sinus externally, such as with shaving.

Carotid sinus massage with terminate approximately 20% of episodes of re-entry supraventricular tachycardia. This vagal maneuver should be avoided or used with caution in the elderly as atherosclerotic plaque formations might become disrupted, and strokes may occur.[13]

There have been propositions made for surgical procedures to treat carotid sinus syndrome, heart failure, hypertension, and insulin resistance. The proposals would be denervation of the carotid sinus for carotid sinus syndrome and carotid body removal for refractory hypertension and heart failure. It has also been suggested to produce baroreceptor electrical stimulation for refractory hypertension and heart failure.

A case study has found that head and neck radiation for treating squamous cell carcinoma of the tongue resulted in orthostatic hypotension due to baroreceptor failure.