Transcription
In this part of the lecture, we will discuss blood pressure regulation mechanisms that are called rapid or fast regulatory mechanisms because they can be activated within a few seconds to minutes. This means that there are also intermediate and long-term mechanisms of blood pressure regulation, but we will not discuss them today. Long-term mechanisms involve substances such as hormones and other factors.
However, when we talk about rapid mechanisms, the system that can respond the fastest is of course the nervous system. So here we will focus on the nervous system and three important mechanisms that are able to significantly influence blood pressure within seconds to minutes. Before I begin discussing the mechanisms themselves, I will first explain the nerve fibers involved and the effects they produce.
So what can you see in this picture? First of all, you see the heart and the aortic arch as well as its ascending and descending parts. Here I have also indicated an extension. The small vessel is intended to represent the entire circulatory system and this should be kept in mind when I describe the mechanisms and effects. In this context, the vessel represents arteries and arteries. Although the same processes also occur in venules and veins just to a lesser extent because veins and venules have lesser receptors and therefore the effects are less pronounced compared to those in arteries and arteries.
What else is shown here is the cardiovascular control center. Anatomically it is actually a single center located in the medulla oblongata. However, functionally and physiologically it can be divided into two parts: the cardioinhibitory center and the cardioaceleratory center. Both of these centers are located in the medulla oblongata. Here I will also show an image where you can see the medulla of longata where in fact many important centers are located. Around this area we have the cardiovascular control center and nearby there is another center that we would also discuss: the vasom motor center. Higher up you can find respiratory center. So this is just a small reminder and a brief revisit of anatomy.
Now let's return to my diagram. So everything is clear about the cardiovascular control center. Let's look at each part separately. The cardioinhibitory center is located in the nuclei of the veagal nerve or nervous vagus. The veagal nerve belongs to the parasympathetic nervous system and from there originate nerve fibers that act on the heart. Since this is the parasympathetic nervous system, there are autonomic ganglia. So additional sinapses in the epherent pathway and the final sinapse which connects to the heart muscle acetylholine is released as the neurotransmitter during stimulation. It acts on M2 receptors in the heart or full name muscerinic type 2 receptors. When this system is activated and acetylholine is released, the effect is that the heart rate decreases and contractility is reduced.
The opposite effect is produced by the cardioaceleratory center. As the name suggests, it is associated with the sympathetic nervous system and heart acceleration. This center is linked to the sympathetic centers located in the spinal cord, specifically from the T1 to T4 segments which innervate the heart. From there the epherence sympathetic pathway continues again with an autonomic ganglia or sinups and at the final signups with the heart norepinephrine or noradrenaline whatever you like to call it is released which acts on beta 1 adinuric receptors. This results in an increase in heart rate and contractile force. Together, these two parts of the cardiovascular control system, determine which branch of the autonomic nervous system, parasympathetic or sympathetic, is dominant at a given moment and thus regulate blood pressure accordingly.
Another important center which I mentioned already here is vazom motor center. As the name suggests, vazo meaning vessels. It regulates blood vessels. This center is also part of the sympathetic nervous system, specifically involving spinal segments from T1 to L3. These nerve fibers from this center primary innervate blood vessels, although some also affect the heart, but here we focus on vessels. The main function of the vasom motor center is vascular regulation. This regulation applies, as I previously said, to arteries, arteries and also veins to a lesser extent. Since it is mediated by the sympathetic system, the main neurotransmitter here will be norepinephrine which acts on alpha 1 adinuric receptors causing vasoc constriction.
Additionally, these fibers can also inervate the adrenal glands. When the vazom motor center is activated, it also activates the adrenal medala leading to the release of adrenaline or epinephrine, again, whatever you like to call it. This further enhances sympathetic effects in both the heart and blood vessels because epinephrine can act on the same adronergic receptors as norepinephrine. So yeah, now that regulation of circulation is clear, we can move on to discussing the rapid mechanisms of blood pressure regulation.
I will start with the first mechanism: the barrow receptor reflex. Barrow receptors are pressure receptors, as the name brow already suggests, and they are located in several places around the heart and in the heart itself. First, they are found in the aortic arch, in both atria, especially the right atrium where they are sensitive to atrial stretch, also in the large veins near the heart, in the pulmonary arteries and veins, and also at the bifurcation of the common and internal caroted arteries. There's also a picture that shows some of the burrow receptor locations I mentioned.
Burough receptors are active when arterial pressure is between 60 and 180 mm mercury. If blood pressure falls below 60 mm mercury, which is of course a lifethreatening situation, borrow receptors become inactive and other life-saving mechanisms take over. The higher the blood pressure, the more the barrow receptors and the bar receptor reflex are activated. When blood pressure decreases, bar receptor activity also decreases and fewer impulses are sent to the brain. It is also important that during physical activity, this reflex is largely suppressed, and this is a pretty smart thing mother nature has done with our body, so that blood pressure can normally increase during exercise and bar receptors don't counteract the increase and reduce blood supply to muscles and the brain during physical activity. So therefore the reflex responds mainly to unexpected changes in the blood pressure, not physiological increases due to exercise. And such changes would be, for example, when a person stands up quickly, blood momentarily pulls in the lower body due to gravity, causing a drop in blood pressure and bar receptor activity with that decreases. On the other hand, when a person drinks a large amount of fluid, blood volume increases, atria and arterial walls stretch, and barrow receptors increase their firing.
Now in this schematic, we are looking at the situation where barrow receptors are activated, meaning when blood pressure is increased. If pressure decreases, the opposite effects will occur. So when blood pressure is high, bar receptors detect this and send impulses to the medulla of longata to the regulatory centers already mentioned. Well, in reality, actually these apherent signals I have drawn here first project to the nucleus solitarius, but this detail can be simplified in this particular course, you don't need it, you need the effects. So the cardioinhibitory center is activated, whereas the cardio acceleratory and the vasom motor centers are inhibited. That's why I have here little minuses. Now this leads to decreased heart rate because the sympathetic nervous system is not active then, but the parasympathetic nervous system is. So we have acetylhaline effect on muscerinic type 2 receptors. So decreased heart rate, reduced contractile force. At the same time, as I said, the sympathetic influence on both the heart and the vessels decreases, and this results in reduced cardiac output. So less ejected blood into arteries, decreased arterial stretch, and gradual reduction of the baro receptor reflex activation. So with this gradual reduction of the baro receptor reflex, baro receptor activity decreases again and the balance shifts back. The cardio acceleratory center and the vasom motor centers become less inhibited, not activated, but less inhibited, and with that heart rate increases and vessels regain some degree of vasoc constriction.
So this is a dynamic regulatory loop that constantly adjusts blood pressure in everyday situations. It is not primarily a pathological mechanism. It is a physiological moment-to-moment regulation system that helps maintain blood pressure stability during daily activities. And it is important to understand it because next we will move on to mechanisms that become especially relevant during pathological conditions.
Next we move on to the cheoceptive reflex. Chemoceptors are also receptors located near the heart. They are found in the vicinity of the aortic arch and the carroted sinus, as I drawn here. Maybe not so elegantly, but understandably, I think. So more precisely, they are located in small bodies adjacent to these vessels, meaning they are outside the vessel wall, and also they receive a very rich blood supply. When the chemo receptor reflex is activated, apherent nerve fibers from these receptors send signals to the vasom motor center, activating it. As a result, vazo constriction of course occurs. The cardiac center may also be activated, but this effect is secondary. The primary effect of chemo receptor activation is the vasom motor center. So that is what we focus on here. So this leads to peripheral vaso constriction, meaning less blood flows to the periphery and more blood remains in the central arteries. You can imagine this like stepping on a garden hose. When you compress it, water flow beyond that point decreases and more water accumulates before the constriction. Similarly, in this case, more blood remains in the central circulation.
Now, what conditions can activate this chemoceptor reflex? First of all, the chemoceptor reflex is activated when the partial pressure of oxygen in the blood decreases. And this will be from all my freemention factors here, the most important factor. Also, when the partial pressure of carbon dioxide increases or when blood pH decreases, meaning acidosis develops. In terms of blood pressure, this reflex becomes active when it falls below 80 mm mercury, which means that in everyday conditions, this mechanism is not really dominant. It mainly comes into play in critical situations. The most common causes that activate the chemo receptor reflex include reduced ventilation, where carbon dioxide accumulates and pH decreases. High altitude conditions, of course, not for the native people, but when a person moves to elevations about 2 and a half thousand to 3,000 m above the sea level without prior adaption. For example, if you're visiting Cusco or Makup Pikchu in Peru. In such cases, oxygen partial pressure drops, even though ventilation may initially increase. In this case, actually peripheral chemo receptors respond by increasing respiratory rate, heart rate, and causing vaso constriction in an attempt to compensate for reduced oxygen availability. So in this case, this is not a life-threatening situation. So central chemo receptors do not respond, but the peripheral ones do.
Now, interestingly and a bit informally, it could be said that in such conditions like the high altitude ones, smokers have a certain advantage. Well, of course, this should not be misunderstood. I don't mean that smoking is good, but chronic smokers and people living in high altitude share one thing in common. Both live under conditions of chronic oxygen deficiency, that is hypoxia, basically, and as a result, their bodies adapt by producing more iritraides. However, this is only an adaption, not a benefit, of course. In smokers, oxygen transport is actually impaired due to carbon monoxide binding to hemoglobin, and increased blood viscosity can make circulation less efficient. So yes, there is an adaption, but it's not a healthy or advantageous one overall.
Continuing further, lung diseases such as severe asthma, pneumonia, or pulmonary edema can impair oxygen diffusion and trigger the reflex. Then shock states, cardiogenic or septic shock, where tissues receive insufficient oxygen, activate the reflex to promote vaso constriction and preserve brain perfusion. Anemia and carbon monoxide poisoning, where oxygen delivery tissues is reduced, even if oxygen partial pressure may appear normal. And finally, premature infants, in whom the chemo receptor reflex is critically important for survival.
And finally, we come to central nervous system is schemic regulation, which acts only under truly critical conditions and primarily involves the vaz motor center itself. If the vazo motor center directly senses the same criteria we discussed earlier, that means decreased oxygen partial pressure or decreased pH, then these changes occur at the level of the vasom motor center itself, and in this case, it becomes immediately and strongly activated. In other words, these same stimuli now act directly on the center, triggering a maximal response. This leads to even stronger peripheral vaso constriction. It is important to understand that if CNS eskeemic regulation is activated, the chemo receptor reflex has already been activated before, but it was not sufficient to correct the situation. Therefore, this mechanism represents a kind of last resort, life-saving response. At this point, blood vessels constrict as much as possible. As a result, even more blood remains in the central arteries and more blood can be directed into the internal carroted arteries, which supply the brain. In critical situations, the body's main goal is to preserve perfusion to the brain and the heart, because if the brain is deprived of blood supply, the outcome is fatal. However, it must also be noted that such extreme vaso constriction can lead to necrosis in peripheral tissues, since blood flow to those areas is severely reduced.
And finally, it should be emphasized that CNS eskeemic regulation is purely a crisis mechanism. It does not occur under normal conditions. It is only activated when the Vazo motor center detects a lifethreatening situation, essentially a matter of life or death. And here it is essentially stated the same way that this mechanism is activated only when the previously described mechanisms can no longer compensate. Although the triggering criteria, partial pressures and pH are the same as in the chemo receptor reflex, there is an important difference to emphasize. The chemo receptor reflex responds, as I said, most strongly to a decrease in oxygen partial pressure. In contrast, CNS eskeemic regulation responds most strongly to increase in carbon dioxide partial pressure. And another thing is the blood pressure level at which CNS eskeemic regulation is activated is below 50 mm mercury, which clearly represents a life-threatening condition and does not occur under normal circumstances.
It should also be noted that sometimes this mechanism can be activated even when arterial pressure is not below 50 mm mercury. This happens when the problem lies within the cranial cavity itself. Since the skull is a closed space, any increase in volume inside it, whether due to brain tissue, for example, tumor, cerebral spinal fluid, for example, menitis, or blood, for example, intraranial hemorrhage. So all these factors will increase intraranial pressure, which can trigger CNS eskeemic regulation. This is because pressure within the cranial cavity remains relatively constant and has a limited capacity to adapt.
It is also important to note that CNS eskeemic regulation is the strongest of all three regulatory mechanisms. Within minutes, it can increase arterial pressure up to 200 mm mercury as the body attempts to redirect as much blood as possible to the brain. At this stage, the organism's priority is clear: maintain brain perfusion at all costs. Even if this leads to necrosis in peripheral tissues, but it is still preferable to meeting the reaper, right? And with that rather dramatic note, we conclude the discussion of these regulatory mechanisms.