How does the mechanism which controls blood pressure in the brain work?

How does the mechanism which controls blood pressure in the brain work?

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I know that pressure is sensed in the skin by mechanoreception mediated by skin receptors. Static pressure stimuli are mainly sensed by slow-adapting fibers connected to receptors like the Merkel discs. Vibratory stimuli are sensed by rapidly adapting receptors like the Pacinian corpuscle.

Blood pressure is also sensed by the body and the brain regulates blood pressure by influencing the peripheral nervous system that can increase or decrease the blood output of the heart.

How are blood pressure differences in the brain sensed and how do these receptors mediate cardiac activity? Are blood pressure differences in the brain sensed by rapidly adapting receptors akin to Pacinian corpuscles?

Blood pressure is sensed in blood vessels by baroreceptors. Baroreceptors are stretch-sensitive nerve fibers located primarily in the aortic arch and carotid sinuses. The baroreceptors send afferent fibers via the glossopharyngeal nerve to the nucleus tractus solitarii in the dorsal medulla in the brainstem. From there, efferent cardiovascular neurons send projections to the medulla and spinal cord. There are also stretch-sensitive receptors in the heart and pulmonary vessels, called cardiopulmonary receptors that use the same nerural connections as the baroreceptors.

The baroreflex loop results in activation of sympathetic or parasympathetic fibers to the heart, the smooth muscle of the peripheral blood vessels, and other organs such as the kidney to maintain arterial pressure at normal levels.

In a simplified scheme, increased pressure stimulates baroreceptors, which attenuates the sympathetic outflow to the peripheral vessels and the heart, restoring pressure to normal levels. The parasympathetic influence will dominate which is mediated by acetylcholine. Conversely, a decrease in pressure relieves the baroreceptors and increases sympathetic outflow. Sympathetic activation causes a release of noradrenaline that leads to vasoconstriction and increased cardiac output and hence an increased blood pressure (see Fig. 1).

Fig. 1. Control of blood pressure. Source: Human Physiology (2011).

- Cougias et al., Med Sci Monit (2010); 16(1): RA1-RA8

The control mechanism in the brain for blood pressure is a endocrine hormone named ADH. This stands for AntiDiuretic Hormone. This hormone is produced by special nerves in the hypothalamus and stored in the posterior pituitary gland. ADH is stimulated by increased blood solute (particles like ions and other molecules) present or decreased blood volume level. When you have adequate hydration, this hormone is actually inhibited. On a very elementary level, it works by stimulating kidney tubule cells to reabsorb water rather than eliminate it. Some drugs also interfere with ADH, most commonly ethanol (drinking alcohol).

Edit: Forgot to add that ADH is also known as Vasopressin, and is also responsible for constricting the blood vessels.

Plan and conduct an investigation to provide evidence that feedback mechanisms maintain homeostasis.

There are 3 major concepts that should be demonstrated by the investigation:


Homeostasis can be thought of as an organism’s fight to stay alive. As the temperature gets colder outside, your body increases circulation to keep your important organs at the right temperature. Another good example is maintaining sugar levels within the bloodstream after a meal. This delicate balance must be maintained for cells to get the nutrients, oxygen, and water that they need while waste products cells produce are removed.

A more formal definition of homeostasis is the ability of an organism to resist change or overcome disruptions in equilibrium in order to maintain a stable internal environment. This is true whether you are talking about a single-celled organism or a blue whale. Typically, internal conditions are contained by either negative feedback loops or positive feedback loops.

Negative Feedback Loop

A negative feedback loop counteracts a stimulus. So, if your blood pressure goes up, a negative feedback loop brings it back down. If your blood sugar rises, a negative feedback loop brings it back down. Negative feedback loops work through a number of different biochemical methods, though the general outline is always the same. Some condition (blood pressure, oxygen level, temperature) causes a process to activate. This process then counteracts the condition that set it off. This serves to keep a number of conditions in your body at a “set” level. While they will go up and down a little bit, they are largely constrained within a set of boundaries. It should be noted that the feedback mechanisms work by reversing the stimulus, whichever direction that stimulus is going. In the blood sugar example, the pancreas releases insulin when blood sugar levels are increasing. This causes blood sugar levels to decrease, reversing the trend back to normal. When blood sugar levels are low and decreasing, another negative feedback mechanism tries to increase blood sugar levels. This reverses the original stimuli until the system is back at equilibrium.

Positive Feedback Mechanisms

Organisms cannot always live in equilibrium, and some process must be carried out until completion. Good examples of this in an individual organism are giving birth, sending signals through nerves, and blood clotting – all of which must be carried out to completion for organisms to survive. Positive feedback mechanisms work in the opposite direction, compared to negative feedback mechanisms. Instead of reversing a stimulus, positive feedback mechanisms enhance or increase the stimulus. Blood clotting is a good example. Injured tissue releases a chemical that causes clotting factors in your blood to activate. These factors activate blood platelets – which start to stick together. These platelets recruit more platelets to the injured site. This process reinforces itself until a blood clot has completely sealed off the wound, stopping the release of chemicals from injured cells. The important aspect of positive feedback mechanisms is that some processes must be completed in order to return to a state of homeostasis.

The take-home message

Don't hesitate to tell your doctor if you notice mood changes or other unpleasant side effects after starting a new medication, says Dr. Zusman. With blood pressure drugs, symptoms such as feeling tired or lightheaded are not unusual during the first week or so, but they often resolve once your body adjusts.

Depression might develop soon after you start a new drug, or possibly months later. It's worth asking your doctor about switching to one of the medications linked to a lower risk of depression if you're not on one of them already. But never stop taking any blood pressure drug abruptly. You can develop rebound hypertension, which raises your risk of a heart attack or stroke, Dr. Zusman stresses. Always make any changes gradually and under your doctor's guidance.

Image: © monkeybusinessimages/Getty Images

Segmental Vascular Resistance

In peripheral circulations, small arterioles (𼄀 μm diameter) are typically the major site of vascular resistance (157). However, in the brain, both large arteries and small arterioles contribute significantly to vascular resistance. Direct measure of the pressure gradient across different segments of the cerebral circulation found that the large extracranial vessels (internal carotid and vertebral) and intracranial pial vessels contribute

50% of cerebral vascular resistance [58,158]. Large artery resistance in the brain is likely important to provide constant blood flow under conditions that change blood flow locally, e.g., metabolism. Large artery resistance also attenuates changes in downstream microvascular pressure during increases in systemic arterial pressure. Thus, segmental vascular resistance in the brain is a protective mechanism that helps provide constant blood flow in an organ with high metabolic demand without pathologically increasing hydrostatic pressure that can cause vasogenic edema.


While short-term changes in BP are regulated by SNS and renin𠄺ngiotensin-aldosterone system (RAAS), long-term BP control is controlled by the kidney.[4] High pressure baroreceptors in the carotid sinus and aortic arch respond to acute elevations in systemic BP by causing a reflex vagal bradycardia that is mediated through the parasympathetic systems and inhibition of sympathetic output from the CNS. Low pressure cardio pulmonary receptors in the atria and ventricles likewise respond to increases in atrial filling by causing tachycardia through inhibition of cardiac SNS, increasing atrial natriuretic peptide (ANP) release and inhibiting vasopressin release.[5𠄷]

Sympathetic regulation also plays a role in long-term BP regulation, as the most important stimulus to renin release in the juxtaglomerular apparatus is through renal sympathetic nerves.

Some of the strongest clinical evidence of sustained neurogenic hypertension comes from studies done in patients with obstructive sleep apnea. Activation of the carotid body chemoreceptors occurs during the apneic spells with arterial desaturation. This causes high BP episodes and a long-term resetting of the chemoreceptor reflex.

The normal control of the arterial BP by SNS is summarized in Figure 2 .

CNS control of sympathetic outflow. Efferent SNS output is the result of integrated actions of several CNS centers, including many areas of the cortex as well as lower centers in hypothalamaus, basal ganglia(especially the locus ceruleus), and circumventricular regions, including the area postrema (AP) and the AV3V region. The critical integrator region is the nucleus tractussolitaries (NTS), which lies in the medulla oblongata. The NTS receives inhibitory afferent signals from the baroreflexes (volume and pressure signals) and stimulatory afferent signals from renal and muscular chemoreceptors (metabolic signals). SNS outflow is ultimately dependent on stimulation of the rostral ventrolateral (the RVLM or vasomotor control center), which is tonically inhibited by the adjacent NTS. Circumventricular regions such as the AP are of particular interest because they have no blood-brain barrier stimulation of the AP by circulating angiotensin II (Ang II) blunts the inhibitory effects of the NTS. Ultimately, RVLM stimulation sends signals via the spinal cord and sympathetic ganglia to regulate heart rate, cardiac stroke volume(SV), and systemic vascular resistance(SVR), which together determine momentary and chronic blood pressure (BP) levels.[71]

How does high blood pressure affect brain function?

High blood pressure is also the strongest risk factor for stroke. The most common cause of stroke is the blockage of the arteries in the brain (ischaemic stroke) and half of these are caused by hardening of the arteries. Another important cause of stroke is the bursting of an artery in the brain, causing what is known as a haemorrhagic stroke, also called bleeding in the brain. Both type of strokes cause brain cell death that can lead to the development of stroke-related or post-stroke vascular dementia.

Narrowing of the blood vessels especially deep inside the brain does not always cause an overt stroke. These very small deep blood vessels can be blocked or have small bleeds (microbleeds). The person may not feel anything wrong at the time, but the gradual accumulation of these changes over the years becomes visible on the brain scan and is called small vessel disease. This is a major contributing factor in the development of subcortical vascular dementia.

What is the mechanism behind high blood pressure in obesity?

Many people with obesity also develop high blood pressure, but the mechanism that leads to this remains unclear. A new study using human tissue samples and mouse models may now have found an explanation.

Share on Pinterest Obesity-related high blood pressure may be due to subtle changes in the cells that line the insides of blood vessels.

Obesity is a top risk factor for elevated blood pressure, though researchers remain unsure as to the exact mechanisms underlying this relationship.

Past research has suggested that to find the mechanism that mediates the relationship between obesity and high blood pressure, scientists should look to the endothelium — that is, the cells that line the insides of blood vessels.

In a new study, researchers from the University of Virginia School of Medicine in Charlottesville have done precisely that. They turned their attention to the endothelium to try to find out exactly how obesity can lead to high blood pressure.

To do so, they studied potential mechanisms in human tissue samples and in mouse models.

They report their findings in a study paper in the journal Circulation.

In their study paper, the investigators explain that to regulate blood flow, vessels dilate and contract as appropriate. This happens due to calcium signaling : Calcium ions communicate with cells, regulating vasodilation by effectively telling the vessels when to dilate.

In obesity, however, calcium signaling within blood vessels appears to be impaired. This affects vasodilation and contributes to high blood pressure.

Yet the mechanism underlying this impairment remains unclear. To learn more about the specific causes behind high blood pressure in obesity, the researchers investigated cellular mechanisms in human tissue samples and mice — under both normal conditions and those that induce obesity.

They found that, normally, a protein called TRPV4 — which is present on the membranes of endothelial cells — allows calcium ions to enter the cells and maintain normal blood pressure.

However, the researchers also found that in obesity, this protein stops “doing its job” — but only in myoendothelial projections , which are specialized extensions of the endothelial cells.

“Under healthy conditions, TRPV4 at these tiny microdomains [the myoendothelial projections] helps maintain normal blood pressure,” explains lead study author Swapnil Sonkusare, Ph.D.

However, when not everything works as it should, these key entry points for calcium become what Sonkusare terms “pathological microdomains.”

“We, for the first time, show the sequence of events that lead to a harmful microenvironment for calcium entry through TRPV4,” he explains.

“I think the concept of pathological microdomains is going to be very important, not just for obesity-related studies but for studies of other cardiovascular disorders as well,” he adds.

According to Sonkusare and team, in obesity, the segments of endothelial cells that hold TRPV4 exhibit an increase in the levels of enzymes that produce peroxynitrite.

This is an ion that silences TRPV4, stopping calcium from entering the epithelial cells. This, in turn, leads to poorer regulation of blood pressure, potentially causing it to become elevated.

Based on this information, researchers may one day be able to come up with a drug that targets this mechanism. Which part of the mechanism should they aim to target, however?

“People asked me, ‘Why don’t you use a drug to directly activate TRPV4?'” says Sonkusare. “But TRPV4,” he explains, “is present in many other tissues, including brain, muscle, and bladder.”

“So if you directly activate TRPV4, you will likely get undesirable side effects.” According to Sonkusare, that is why “[t]he better approach would be to target the specific events that reduce TRPV4 function in obesity.”

In this case, he says, it may be helpful to act directly on either peroxynitrite or the enzymes that produce it. This approach might help regulate blood pressure without causing unwanted effects.

“We, for the first time, identify peroxynitrite as the precise oxidant molecule that increases blood pressure in obesity. The next step would be to design drugs that specifically target peroxynitrite and provide therapeutic benefit,” he explains.

“If we are able to design the appropriate compounds, we might be able to treat hypertension in [people with obesity].”

– Swapnil Sonkusare, Ph.D.

The researchers also note that their recent findings were possible due to the use of innovative, sophisticated techniques that allow real-time visualization of calcium and TRPV4 interactions in very small blood vessels.

Sonkusare concludes: “Historically, researchers have studied larger blood vessels that don’t control blood pressure. Because of our unique techniques, we are able to study the microdomains in very small arteries that control the blood pressure. So our technical ability allows us to obtain these unique insights.”

Blood Pressure Control By Baroreceptors

The mean arterial pressure (MAP), also considered as the perfusion pressure, is taken as the pressure difference between the arteries and the veins. The regulation of blood pressure is done in order to maintain the MAP.

The MAP dictates the amount of oxygen and nutrients that is supplied by the blood vessels and the waste that is carried away from the tissues.

Regulation Of Blood Pressure

The body has the ability to counteract long term as well as short term changes in blood pressure. The long term pressure changes cause the body to respond through the activation of renin-angiotensin system.

Rapid/short term changes in blood pressure compel the body to activate the following receptors:

  • Baroreceptors are present on the arch of aorta and carotid sinus
  • Chemoreceptors are present in the carotid sinuses, arch of aorta and medulla oblongata
  • Atrial receptors are present on the wall of right atrium


The baroreceptors are the pressure sensing bodies. They are also called stretch receptors.They are modified nerve endings attached to the cytoskeleton present within the nerve endings. The receptors are sensitive to rapid offsets in blood pressure. The baroreceptors are densely situated on the walls of the arch of aorta and the carotid sinus. The carotid sinus is present on the base of internal carotid artery at the level of bifurcation of the common carotid artery. The sinus area is slightly dilated as the tunica media which is normally comprised of muscles, is relatively thin. The tunica adventitia, on the other hand, is thicker than usual. This is the layer of the blood vessels where the nerve receptors are situated. Same is true for the location of baroreceptors on the arch of aorta.

Rapid offsets in pressure can occur, for example, in a previously standing person who suddenly sits down. During the process, a large volume of blood is shifted from the peripheral to the central regions of the body. Consequently, a large volume of blood enters the heart and this volume overload or increased preload causes the heart to increase its cardiac output. A simultaneous increase in blood pressure will also be observed with increase in cardiac output. The increase in blood pressure is registered by the baroreceptors.

Similarly, a drop in blood pressure is registered by the baroreceptors when the person stands up suddenly from a sitting position. High blood pressure in the blood vessels causes stretch of these receptors which results in movement of sodium ions into the nerve endings, thereby, initiating an action potential.

These baroreceptors have a baseline firing pattern. That means they have an intrinsic potential to generate action potentials at a particular frequency at all times. This frequency is increased when the baroreceptors receive a stretch stimulus secondary to increase in blood pressure. The carotid sinuses increase their rate of impulse generation when the pressure in them builds up to values greater than 50 mm Hg. Below this threshold pressure, the carotid baroreceptors fail to initiate an action potential. On the other hand, the arch of aorta can record drops in blood pressure up to 30 mm Hg. The upper limit for blood pressure, after which the frequency of action potential stops increasing, is 175 mm Hg. The normal MAP is calculated to be 93 mm Hg. At this pressure, the baroreceptors are believed to be the most sensitive and even slight changes in pressure will result in rapid firing of action potentials.

At blood pressures lower than 30 mm Hg, the chemoreceptors come into play. The chemoreceptors function by sensing the arterial concentration of carbon dioxide, oxygen, Ph and other metabolites . They do not detect changes in blood pressure.

Baroreceptor Reflex

The baroreceptor reflex like other reflex arcs is comprised of three units:

  • Afferent nerve carrying impulses from the receptors
  • Central processing unit
  • An efferent nerve that innervates the effector

Afferent impulses from the carotid sinus are carried by the Herring nerve, a branch of Glossopharyngeal nerve (CN-9). In the case of baroreceptors present on the arch of aorta, the Vagus nerve (CN-10) is the afferent nerve that carries impulses to the spinal cord. Both, the Vagus nerve and the Glossopharyngeal nerve, feed impulses from the baroreceptors into the nucleus of tractus solitarius. These nuclei are situated in the medulla of the spinal cord and their job is to process the incoming afferent impulses. Also within the Medulla and lower 1/3rd of the Pons, there are vasoconstricting center, the vasodilatory center and the cardio-inhibitory center. These centers receive processed impulses from the nucleus of tractus solitarius and from here efferent impulses in the form of sympathetic and parasympathetic nerves arise. Impulses are carried to the heart via the parasympathetic Vagus nerve. Sympathetic impulses travel down the intermedio-lateral segment of the spinal cord and give rise to efferent motor spinal nerves which enter the sympathetic ganglion running parallel to the spinal cord. Postganglionic sympathetic nerves ultimately supply the heart and the peripheral vasculature. Another preganglionic sympathetic nerve also supplies the adrenal medulla which results in the release of epinephrine and norepinephrine, which further contribute in enhancing the sympathetic activity. The end result is either an increase or decrease in the blood pressure, thereby correcting the disturbance in hemodynamics of the body. This phenomenon is also referred to as the buffering effect, since the change in pressure is buffered back to normal. The Vagus and Glossopharyngeal nerves, because of the same reason, are therefore known as the buffering nerves.

Factors Responsible For Change in Mean Arterial Pressure

MAP = Heart Rate x Cardiac Output

Whereas, CO = SV (stroke volume) x TPR (total peripheral resistance)

Therefore, MAP = HR x SV x TPR

The stroke volume is altered by altering the force of contractility of the heart muscles. The sympathetic nerves supplying the heart muscles affect the stroke volume. The parasympathetic nerves supplying the SA and AV node are responsible for producing changes in heart rate. The TPR can be increased or decreased by changing the diameter of peripheral vasculature which is under the control of the sympathetic nervous system.

Effects of Baroreceptors in Various Conditions

Due To Changes In Blood Pressure

  • Reduced Blood Pressure: Reduction in blood pressure will result in a decrease in the number of afferent impulses from the baroreceptors. The sympathetic activity will increase and as a result, the TPR, HR and the stroke volume will all increase. At the same time, the parasympathetic input will taper down. All these changes will result in increasing the blood pressure back to normal.
  • Increased Blood Pressure: This happens in situations like exercise or stress. Increased blood pressure will result in stretching of the stretch receptors. This increases the frequency of afferent impulses. Sympathetic supply will decrease and the parasympathetic system will take over. Finally, the blood pressure is decreased back to normal.

Due To Changes In Cardiac Output

  • Decreased Cardiac Output: Occurs in situations of vomiting, diarrhea, hemorrhage etc. As a result of these, both the volume, and therefore pressure of the blood decreases. Afferent impulse firing of the baroreceptors decreases. As a consequence, there’s a sympathetic overflow which causes an increase in HR, TPR and SV. Due to an increase in these parameters, the blood pressure is raised back to normal.
  • Increased Cardiac Output: There’s an increased impulse generation from the baroreceptors due stretch caused by increased volume of blood. This increased afferent input from the baroreceptors results in activation of the PANS. Once activated, the parasympathetic nervous system decreases the blood pressure back to normal.

Massaging The Carotid Sinus

Massaging the carotid sinuses physically increases the pressure on the baroreceptors present there. The carotid baroreceptors respond by increasing the rate of afferent impulse firing. The sympathetic system will be shut down and the parasympathetic system is activated. This results in decrease in blood pressure of the body.

Carotid massage by activating parasympathetic nervous system increases AV nodal refractory period, thereby decreasing AV node conduction and finally decreasing Heart Rate. This is the reason Carotid sinus massage is the initial menuever used in the treatment of paroxysmal supra-ventricular tachycardia.

Stenosis Of The Carotids

Stenosis of carotids proximal to the sinus or obstruction of the carotids due to atherosclerosis will cause the baroreceptors to register a decrease in pressure. Therefore, sympathetic system activation follows. Increased sympathetic activity causes a resultant increase in blood pressure. This increase in blood pressure may cause hypertension in an otherwise normal person.

Baroreceptor responses are summarized in the table below

It’s important to understand that control of BP by baroreceptor is a short term regulation of blood pressure. Any short term derangements are dealt via the baroreceptor response, whereas long term control of the BP is controlled via the RAAS (Renin Angiotensin Aldosterone System).

The baroreceptors also have the ability to adapt to chronic changes in blood pressure. If the mean pressure is changed over time to a new value, the baroreceptors will start using that MAP as the baseline. Any subsequent blood pressure changes will then be rectified keeping in view the new baseline value of MAP.

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Written by Mobeen Syed
October 19, 2016 . Leave a Comment

Long-term control of arterial blood pressure

Two concepts for the long-term regulation of arterial pressure were considered in this review, the neural control hypothesis and the volume regulation hypothesis. The role of the nervous system and fluid volume regulation are intertwined in a way that has made it difficult to experimentally evaluate their separate contributions in the long-term regulation of arterial pressure. Nevertheless, from a substantial body of work related to the neural control of cardiovascular function, it appears that the ability of the nervous system to control arterial pressure is limited to the detection and correction of rapid short-term changes of arterial pressure. A long and exhaustive search has yet yielded no new neural mechanisms beyond the classic sinoaortic baroreceptors that can detect changes of arterial pressure. The baroreceptor mechanisms are of great importance for the moment-to-moment stabilization of arterial pressure, but because they do not possess sufficient strength and because they reset in time to the prevailing level of arterial pressure, they cannot provide a sustained negative feedback signal to provide long-term regulation of arterial pressure in face of sustained stimuli. This is not to say that the nervous system cannot affect the long-term level of arterial pressure. A distinction is made here between the many factors that can influence the long-term level of pressure and those that actually serve to detect changes of pressure and serve to maintain the level of pressure within a narrow range over the period of our adult lifetime. In this sense, there is evidence that in genetically susceptible individuals, environmental stresses can influence the long-term level of arterial pressure via the central and peripheral neural autonomic pathways. It is inappropriate, however, to view the nervous system as a long-term controller of arterial pressure because there is yet no evidence that the CNS can detect changes of arterial pressure nor changes in total body sodium and water content over sustained periods whereby it could provide an adequate long-term normalization of such error signals. In contrast, evidence has grown in support of the renal pressure-diuresis volume regulation hypothesis for the long-term control of arterial pressure over the past decade. An enhanced understanding of the mechanisms of pressure diuresis-natriuresis coupled with studies exploring how changes of vascular volume can influence vascular smooth muscle tone provide a compelling basis for this hypothesis of long-term arterial pressure regulation. This overall concept is represented and summarized in Figure 12.(ABSTRACT TRUNCATED AT 400 WORDS)

Regulating Your Blood Pressure Over the Long Term

Over the long term, your kidneys are primarily responsible for blood pressure. In fact, many blood pressure lowering medications work by triggering the kidneys to release excess sodium and fluid. When working properly, this fluid regulation system keep blood pressure relatively constant over the years (ref 5). When your blood pressure is high, hormones are released to signal increased urination, lowering blood volume and blood pressure (ref 2). When blood volume and pressure is too low, hormones secreted from your brain tell your kidneys to retain sodium and water, increasing blood volume and blood pressure (ref 5). Problems with this system can lead to high blood pressure, which increases your risk of heart attack and stroke.

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