The baroreceptor reflex is initiated by baroreceptors (also called pressoreceptors) in the walls of blood vessels and corresponds to an automatic response of the circulatory center to sudden changes in blood pressure. In case of suddenly lowered blood pressure due to blood loss, the reflex ensures blood supply to vital organs with centralization of the circulation. This is the case, for example, in hypovolemic shock.
What is the baroreceptor reflex?
The baroreceptor reflex begins with a change in blood pressure, which is transmitted by the baroreceptors to the central nervous system in the form of a stimulus. Baroreceptors are mechanoreceptors in the walls of blood vessels. Mechanoreceptors are sensory cells for registering pressure stimuli. In the wall of blood vessels, the receptors measure blood pressure, so especially blood pressure changes. Like all receptors in the body, they convert stimuli into electrical excitation and thus translate them into the language of the nervous system. They send signals in the form of nerve excitation via afferent pathways to the central nervous system, from where changes in total peripheral resistance and cardiac output are initiated as needed. In this way, the baroreceptors mediate, among other things, the so-called baroreceptor reflex. Reflexes are automatic and volitionally uncontrollable responses that the nervous system makes to certain stimuli. The beginning of a reflex arc is always a specific stimulus that stimulates the same response from the nervous system. The baroreceptor reflex begins with a change in blood pressure, which is transmitted by the baroreceptors to the central nervous system in the form of a stimulus. This stimulus transmission triggers an automated response to regulate blood pressure levels and thereby maintain circulation.
Function and task
Baro- or pressoreceptors are located in greater numbers in the carotid sinus and in the region of the aortic arch. The pressoreceptors located there are P-D receptors. These are potential-differential receptors, which correspond to a combination of differential and proportional receptors. PD receptors increase their action potential frequency when a change in stimulus is detected and maintain this frequency as long as the stimulus persists. Thus, like the differential receptor, they respond to stimulus changes. Unlike differential receptors, however, they not only report the stimulus change, but also signal the exact stimulus duration to the central nervous system, as is also the case for proportional receptors. Only at the end of the stimulation does their action potential frequency drop back below the resting value. Thus, the receptors in the vessel walls measure absolute blood pressure, register changes in blood pressure, and also perceive the rate of change, being capable of registering blood pressure amplitude and heart rate. They send these measurements to the circulatory center within the medulla oblongata via afferents. Blood pressure is regulated in this center via the principle of negative feedback. When blood pressure increases, the parasympathetic nervous system is reflexively activated from here via the vagus nerve. This results in a decrease in sympathetic activity. This process has a negative chronotropic effect on the heart. Thus, in the resistance vessels of the body periphery, the tone in the vascular smooth muscles changes. Conversely, when the receptors register a decrease in blood pressure, the circulatory center inhibits the activity of the parasympathetic nervous system. This simultaneously increases the activity of the sympathetic nervous system, since the two areas are antagonistic to each other and regulate each other in this way. As a consequence of the falling parasympathetic tone and the increased sympathetic activity, the heart rate eventually increases. Total peripheral resistance also increases as the smooth muscle of the resistance vessels is brought into contraction. In addition, increased venous return occurs.
Diseases and complaints
For example, the baroreceptor reflex plays a role in clinical practice in the setting of hypovolemic shock during major blood loss, which can lead to a sharp drop in blood pressure. Elongation of the aortic wall decreases during such an event, which causes baroreceptor activity to decrease, thereby causing them to send fewer signals to the medulla oblongata.Without baroreceptor-mediated inhibition, the neurons located there send increased signals to the heart muscle and to the individual veins and arteries. In a response, the heart rate accelerates and the heart allows more blood to exit accordingly. All arterioles and veins contract, allowing less blood to flow to the tissues. Most of the blood is thus directed to the vital organs during large blood losses. The redistribution of blood is achieved in the context of shock symptomatology primarily through the release of epinephrine and is mediated largely through beta-adrenoreceptors. In hypovolemic shock, treatment focuses on normalizing blood volume to break the shock spiral. To normalize blood pressure, patients are given infusion solutions through large-lumen peripheral access lines that increase the volume in the vessels. Volume replacement is intended to compensate for hypovolemia but must not result in significant hypervolemia. All major blood losses also require causative treatment focused on stopping the bleeding. In this context, the baroreceptor reflex is a symptom of shock that ensures blood supply to the vital organs and, to this end, retains blood from less important tissues. Since the “less important” tissues in the shock situation are no longer supplied with sufficient oxygen and nutrients until the blood pressure stabilizes, individual tissues can become necrotic, i.e. die, as a result of a prolonged state of shock. For this reason, rapid volume replacement is absolutely essential after major blood loss. As blood pressure normalizes, the symptoms of shock subside. From this point on, the vital blood reaches all tissues again. Thus, volume replacement serves to ensure perfusion.