Table of Contents
Regulation of Arterial Blood Pressure
Arterial blood pressure is regulated by a variety of feedback mechanisms involving specific receptors present in blood vessels and the heart. These receptors send signals to the specific areas of the brain that then send impulses to the autonomic nervous system.
Rapid-acting nervous system-mediated mechanisms of action for the regulation of blood pressure:
- Baroreceptor feedback mechanism
- Central nervous system ischemic mechanism
- Chemoreceptor mechanism
Intermediate-acting mechanism for control of blood pressure:
- Renin-angiotensin vasoconstrictor mechanism
- Stress relaxation of the vasculature
- Fluid shift across the capillary for adjustment of blood volume
The long-term mechanism for control of blood pressure:
- Renal blood volume pressure control mechanism
Autonomic Nervous System
The Autonomic Nervous System consists of the sympathetic and parasympathetic nervous system. While sympathetic stimulation plays a major role in the regulation of arterial blood pressure, the parasympathetic system is equally essential in the regulation of cardiac activity.
Sympathetic nervous system
The vasomotor fibers of the sympathetic nervous system arise from the thoracic and the first 2 lumbar spinal nerves. They pass through the sympathetic chain and innervate the vasculature, heart, and viscera through specific sympathetic nerves. In addition, they innervate the peripheral vasculature through the spinal nerves.
The sympathetic innervation of the small arteries and arterioles enables an increase in peripheral resistance with a concomitant rise in arterial blood pressure. Sympathetic stimulation causes vasoconstriction in veins with a decreased volume of blood. This causes an increase in heart rate, the force of cardiac contractility, and stroke volume. The overall result is a rise in cardiac output.
Sympathetic fibers are mostly vasoconstrictive in nature, but a few fibers are vasodilatory depending upon the type of organ and tissues. Norepinephrine neurotransmitter is secreted by the vasoconstrictor sympathetic nerve fibers. These acts on the alpha receptors of the vascular smooth muscles to cause vasoconstriction.
When the sympathetic vasoconstrictor signals are sent to the vascular smooth muscles, the impulses are also transmitted to the adrenal medulla. The adrenal medulla secretes epinephrine and norepinephrine. While norepinephrine only causes vasoconstriction, epinephrine can sometimes cause vasodilation via activation of beta receptors.
Parasympathetic nervous system
As discussed earlier, the parasympathetic fibers are important in controlling the heart rate. The vagus nerve carries parasympathetic fibers to the heart. Its stimulation causes a decrease in heart rate as well as the cardiac contractility.
The vasomotor center is located bilaterally in the reticular substance of the medulla and the lower one-third of the pons. The impulses are transmitted to the autonomic nerve fibers through the spinal cord.
The vasomotor area is further subdivided into the following regions:
- The vasoconstrictor area, also known as C1, distributes its fibers throughout the cord. The neurons in these fibers release norepinephrine and activate the vasoconstrictor fibers of the sympathetic nervous system. Under normal conditions, this area continuously stimulates these fibers at a rate of 1–2 impulses per second. This continuous firing is called sympathetic vasoconstrictor tone and the partial state of constriction of the blood vessels is called vasomotor tone.
- The vasodilator area, also referred to as A1, sends inhibitory signals to the vasoconstrictor area, hence causing vasodilation.
- The sensory area, also called A2, receives sensory signals from the glossopharyngeal and vagus nerves. The output signals control the activities of the vasoconstrictor and vasodilator area.
The lateral portion of the vasomotor center controls cardiac activity by sending excitatory impulses to the sympathetic fibers, while the medial portion sends signals via the vagus nerve, thereby decreasing cardiac activity.
Control of vasomotor center by higher nervous centers
The vasomotor center is under control of higher nervous centers:
- The reticular substance of the pons, mesencephalon, and diencephalon can either excite or inhibit the vasomotor center.
- The posterolateral portion of the hypothalamus causes excitation of the vasomotor center while the anterior portion can either cause excitation or inhibition.
- Different parts of the cerebral cortex such as the motor cortex, anterior temporal lobe, orbital areas of the frontal cortex, amygdala, anterior cingulate gyrus, and septum can either excite or inhibit the vasomotor center.
Reflex Mechanisms for Maintaining Normal Arterial Pressure
Multiple subconscious reflex mechanisms are present in our body to keep arterial pressure under control. Almost all mechanisms work by a negative feedback mechanism as follows:
The Baroreceptor Reflex
The baroreceptor reflex, also known as the pressure buffer system, is the most important reflex mechanism for the control of rapid changes in the arterial pressure.
Note: Baroreceptors are also known as the stretch receptors and are present in the wall of the great arteries. They are abundant in the internal carotid artery above the level of bifurcation in an area is known as the carotid sinus. The aortic arch also has a large number of baroreceptors.
Carotid sinus baroreceptors are less sensitive to pressures in the range of 0–60 mm Hg, but are stimulated by pressure above 60 mm Hg. Aortic baroreceptors are sensitive to pressures above 30 mm Hg. Since the baroreceptor system opposes either increases or decreases in arterial pressure, it is called a pressure buffer system and the nerves from the baroreceptors are called buffer nerves.
The long-term regulation of mean arterial pressure by baroreceptors requires interaction with additional systems principally involving the renal-body fluid-pressure control system along with associated nervous and hormonal mechanisms.
Once stimulated, baroreceptors send signals through the sinus of Hering’s nerve, which is a branch of the glossopharyngeal nerve, which finally reaches the sensory area of the vasomotor area of the brain. The response is the inhibition of the vasoconstrictor area and the excitation of the vagal nerve. This leads to vasodilation of arterioles and veins with decreased heart rate and decreased force of cardiac contractility.
When the arterial blood pressure goes back to normal limits, the baroreceptors stop sending signals and the reflex response is stopped by the negative feedback mechanism. The baroreceptors respond very rapidly to changing arterial pressure. The rate of impulse transmission is greater when the pressure is increasing such as the systole and decreases when the pressure is dropping as in the diastolic phase.
Reduction in arterial blood pressure
A sudden change in posture, for example, when a person stands up from the supine or seated position, may result in a drop in arterial pressure. Baroreceptors sense the reduction in arterial pressure and activate the sympathetic system to cause vasoconstriction which increases arterial pressure. Ultimately this prevents any sudden loss of consciousness with syncope due to low arterial pressure.
Long-term pressure changes will cause the baroreceptor system to become non-functional despite an increase in arterial blood pressure. Within only 1-2 days of normal blood pressure fluctuations, the baroreceptor system can reset the current pressure.
The Chemoreceptor Reflex
Chemoreceptors are also present in the wall of the arch of the aorta and carotid arteries where they form the carotid and aortic bodies respectively.
Unlike the baroreceptors, the chemoreceptors are sensitive to changes in concentration of oxygen, carbon dioxide, and hydrogen ions in the arterial blood. Carotid and aortic bodies are supplied with a nutrient artery. Drops in arterial pressure lower the blood supply which chemoreceptors sense as a lack of oxygen with a build-up of carbon dioxide and hydrogen ions in the blood.
Chemoreceptors follow the same pathway as that of the baroreceptor reflex.
The chemoreceptor reflex is not as sensitive as baroreceptors in controlling the arterial pressure as the chemoreceptors are not activated unless the arterial pressure falls below 80mm Hg.
When the walls of the atria are stretched, atrial natriuretic hormone (ANF) is produced in the heart. ANF increases the volume dilatation of the peripheral arterioles and increased urine production. This response is more potent in the afferent arterioles of the kidney. The glomerular pressure rises, causing more filtration of fluid and the production of more urine. Signals are simultaneously sent to the hypothalamus to stop the release of antidiuretic hormone (ADH). Thus less water is reabsorbed from the kidneys causing arterial pressure to come back to the normal range.
Abdominal compression reflex
Stimulation of the vasoconstrictor area of the brain causes an excitatory signal to be sent to the sympathetic nerves, while the brain stem simultaneously sends impulses to the abdominal skeletal muscles of the body. The basal tone of the abdominal muscles increases, which causes compression of the veins. This increases venous return to the heart, providing more blood to be pumped by the ventricles.
Central nervous system ischemic response
Reductions in arterial pressure below 60 mm Hg may lead to cerebral ischemia due to reduced blood flow to the vasomotor area.
Carbon dioxide is the major signaling molecule exciting the vasomotor area neurons to send signals activating the sympathetic nervous system. Other substances such as lactic acid and other acidic substances also contribute to the production of such a response.
Sympathetic excitation causes full occlusion of the peripheral arterioles that may last for as long as 10 minutes with a concomitant rise in arterial pressure as high as 250 mm Hg. The highest degree of response is produced when the arterial pressure falls to 20 mm Hg. Accordingly, the central nervous system ischemic response is sometimes called the ‘last-ditch stand’.
When the arterial pressure falls, intrinsic reactions in the kidneys themselves cause many of the pro-renin molecules in the juxtaglomerular cells to convert to renin. Then most of the renin enters the renal blood and passes out of the kidneys to circulate systemically.
During its persistence in the blood, angiotensin II has 2 principal effects elevating arterial pressure:
- The 1st occurs rapidly and involves vasoconstriction in many areas of the body. This occurs more intensely in the arterioles than in the veins to ultimately raise arterial pressure.
- The 2nd mechanism by which angiotensin II increases the arterial pressure is to decrease both salt and water excretion by the kidneys. The long-term effect of this is even more powerful than the acute vasoconstrictor mechanism in eventually raising the arterial pressure.
Angiotensin II causes the kidneys to retain both salt and water in 2 major ways:
- Angiotensin II acts directly on the kidneys to cause salt and water retention.
- Angiotensin II causes the adrenal glands to secrete aldosterone, which increases salt and water reabsorption by the kidney tubules.
Ambulatory Blood Pressure Monitoring
Measurement of arterial blood pressure at regular intervals over a minimum time window of 24 hours is called ambulatory blood pressure measurement. A digital monitor is attached to the waist through an abdominal belt and the cuff is tied around the arm. The patient is asked to move around and perform routine daily tasks. Nocturnal blood pressure is usually 10% lower than daytime blood pressure. The disappearance of the decline in blood pressure at night of less than 10% from daytime is suggestive of increased cardiovascular risks and renal insufficiency.
The goals of monitoring ambulatory blood pressure are:
- To avoid the effect of white coat hypertension: some patients become anxious and panic whenever their blood pressure is measured.
- To follow the variation in blood pressure during the day and risk assessment related to coronary heart disease risk. This is recommended before initiating an anti-hypertensive drug.
- To see the response to medications if a patient is on multiple anti-hypertensive drugs.