Mechanism of activation of baroreceptors

Baroreceptors are activated in response to stretch produced in the vessel wall. When the pressure is low, the receptors are inactivated and when escalates, there is an increased vessel elasticity in the wall due to distension between carotid and aortic sinuses. When the blood pressure is normal, baroreceptors report blood pressure information for each second and the baroreflex actively modulates autonomic activity. Both sympathetic plus parasympathetic nervous arrangements are involved and have opposing effects on the regulation of blood pressure. Sympathetic neurons increase blood pressure by increasing peripheral resistance then cardiac yield and causing arterial vasoconstriction. Parasympathetic activation acts oppositely to decrease blood pressure.

Increase pressure results in increase action potential within the baroreceptors. This increased stimulus of the tractus solitarius nucleus leads to inhibition of sympathetically increased peripheral resistance which results in vasodilation and lowering of blood pressure. The opposite is seen when mean arterial pressure drops. There is a decrease in action potential and lessened stimulus of nucleus tractus solitarius increased sympathetic activity causing increased peripheral resistance and vasoconstriction ultimately allowing the baroreflex to elevate blood pressure. Similarly, cardiopulmonary baroreceptors are activated in response to enhance blood capacity and mean arterial pressure also increase their action potential which inhibits sympathetic activity resulting in decreased cardiac output. However, to lower the blood volume sympathetic activity of the kidney rises increasing renal outflow and urine production.

The function of baroreceptor reflux:
The main function of baroreflex is to stabilize the perfusion pressure despite disturbances in circulatory homeostasis. Two factors determine baroreceptor reflex function-

The pressure changes to which the reflex responds most effectively (the operating point of the reflex).

The magnitude of reflex response.

Rapid blood pressure variations as seen in orthostatic hypertension are rapidly detected by arterial baroreceptors due to changes in arterial wall stretching. When the pressure drops, there is decreased wall stretching, decrease action potential, increase sympathetic activity, increased vasoconstriction, and hence increase blood pressure. The opposite occurs when the pressure rises. Similarly, cardiopulmonary receptors function to maintain blood volume. Increased salt and water resorption within the kidneys elevate the blood volume.

Cardiopulmonary receptors are also associated with body position changes. This property of baroreflex is exploited to treat resistant hypertension in which a device is implanted that electrically stimulates baroreceptors in the carotid sinus region. Similarly, the ability of baroreceptor reflex to reduce the sympathetic nervous system movement can be used to treat chronic heart failure. As in chronic heart failure, there is increased sympathetic activity which predisposes the individual to arrhythmia and death.

Measurement of baroreceptor reflex sensitivity (BRS):
Alteration in the baroreceptor reflux results in increased sympathetic activity with a significant reduction in parasympathetic activity. This forms the basis of many cardiovascular diseases.

Thus, regulation of baroreflex is an important factor in managing cardiac disease patients.

Regular measurement of baroreflex is done in such patients. The most relevant methods developed to measure BRS includes-

Initially, angiotensin was used which was later replaced by phenylephrine, an Alpha-adrenoreceptor agonist.

Valsalva maneuver- it provokes elevations in intrathoracic and intraabdominal pressure by stroking. It is natural means of activating baroreflex.

Neck chamber- it is a mechanical means to activate or deactivate baroreceptors by applying a certain amount of pressure in the neck chamber. Increase pressure in the neck chamber is sensed as decreased arterial pressure by the baroreceptors. This causes sympathetic heart stimulus and increases blood pressure.

There exist some limitations to each of the methods. However recent proposals were presented to overcome these limitations.

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