Baroreceptor

Baroreceptor

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Baroreceptors are a type of mechanoreceptor sensory neuron that are excited by a stretch of the blood vessel. Thus, increases in the pressure of blood vessel triggers increased action potential generation rates and provides information to the central nervous system. This sensory information is used primarily in autonomic reflexes that in turn influence the heart cardiac output and vascular smooth muscle to influence vascular resistance.[1] Baroreceptors act immediately as part of a negative feedback system called the baroreflex,[2] as soon as there is a change from the usual mean arterial blood pressure, returning the pressure toward a normal level. These reflexes help regulate short-term blood pressure. The solitary nucleus in the medulla oblongata of the brain recognizes changes in the firing rate of action potentials from the baroreceptors, and influences cardiac output and systemic vascular resistance.

Baroreceptors can be divided into two categories based on the type of blood vessel in which they are located: high-pressure arterial baroreceptors and low-pressure baroreceptors (also known as cardiopulmonary[3] or volume receptors[4]).

Arterial baroreceptors are stretch receptors that are stimulated by distortion of the arterial wall when pressure changes. The baroreceptors can identify the changes in both the average blood pressure or the rate of change in pressure with each arterial pulse. Action potentials triggered in the baroreceptor ending are then directly conducted to the brainstem where central terminations (synapses) transmit this information to neurons within the solitary nucleus[5] which lies in the medulla. Reflex responses from such baroreceptor activity can trigger increases or decreases in the heart rate. Arterial baroreceptor sensory endings are simple, splayed nerve endings that lie in the tunica adventitia of the artery. An increase in the mean arterial pressure increases depolarization of these sensory endings, which results in action potentials. These action potentials are conducted to the solitary nucleus in the central nervous system by axons and have a reflex effect on the cardiovascular system through autonomic neurons.[6] Hormone secretions that target the heart and blood vessels are affected by the stimulation of baroreceptors.

At normal resting blood pressures, baroreceptors discharge with each heart beat. If blood pressure falls, such as on orthostatic hypotension or in hypovolaemic shock, baroreceptor firing rate decreases and baroreceptor reflexes act to help restore blood pressure by increasing heart rate. Signals from the carotid baroreceptors are sent via the glossopharyngeal nerve (cranial nerve IX). Signals from the aortic baroreceptors travel through the vagus nerve (cranial nerve X).[7] Carotid sinus baroreceptors are responsive to both increases or decreases in arterial pressure, while aortic arch baroreceptors are only responsive to increases in arterial pressure.[5] Arterial baroreceptors inform reflexes about arterial blood pressure but other stretch receptors in the large veins and right atrium convey information about the low pressure parts of the circulatory system.

Baroreceptors respond very quickly to maintain a stable blood pressure, but their responses diminish with time and thus are most effective for conveying short term changes in blood pressure. In people with essential hypertension the baroreceptors and their reflexes change and function to maintain the elevated blood pressure as if normal. The receptors then become less sensitive to change.[8]

Electrical stimulation of baroreceptors has been found to activate the baroreflex, reducing sympathetic tone throughout the body and thereby reducing blood pressure in patients with resistant hypertension.[9]

The low-pressure baroreceptors, are found in large systemic veins, in pulmonary vessels, and in the walls of the right atrium and ventricles of the heart (the atrial volume receptors).[4] The low-pressure baroreceptors are involved with the regulation of blood volume. The blood volume determines the mean pressure throughout the system, in particular in the venous side where most of the blood is held.

The low-pressure baroreceptors have both circulatory and renal effects; they produce changes in hormone secretion, resulting in profound effects on the retention of salt and water; they also influence intake of salt and water. The renal effects allow the receptors to change the mean pressure in the system in the long term.

Baroreceptors are integral to the body's function: Pressure changes in the blood vessels would not be detected as quickly in the absence of baroreceptors. When baroreceptors are not working, blood pressure continues to increase, but, within an hour, the blood pressure returns to normal as other blood pressure regulatory systems take over.[10]

Baroreceptors can also become oversensitive in some people (usually the carotid baroreceptors in older males). This can lead to bradycardia, dizziness and fainting (syncope) from touching the neck (often whilst shaving). This is an important cause to exclude in men having pre-syncope or syncope symptoms.

Whether arterial baroreceptors play a role in setting the long-term level of mean arterial pressure (MAP) has been debated for more than 75 years. Because baroreceptor input is reciprocally related to efferent sympathetic nerve activity (SNA), it is obvious that baroreceptor unloading would cause an increase in MAP. Experimental proof of concept is evident acutely after baroreceptor denervation. Chronically, however, baroreceptor denervation is associated with highly variable changes in MAP but not sustained hypertension. The ability of baroreceptors to buffer imposed increases in MAP appears limited by a process termed \"resetting,\" in which the threshold to fire shifts in the direction of the pressure change and if the pressure elevation is maintained, it leads to a rightward shift in the relationship between baroreceptor firing and MAP. The most common hypothesis linking baroreceptors to changes in MAP proposes that reduced vascular distensibility in baroreceptive areas would cause reduced firing at the same pulsatile pressure and, thus, reflexively increase SNA. This review focuses on effects of baroreceptor denervation in the regulation of MAP in human subjects compared with animal studies; the relationship between vascular compliance, MAP, and baroreceptor resetting; and, finally, the effect of chronic baroreceptor unloading on the regulation of MAP.

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]

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 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.

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.

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] 59ce067264

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