Neural Controls of Blood Vessels

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Chapter: Anatomy and Physiology for Health Professionals: Vascular System

1. Describe baroreceptor reflexes that control blood pressure changes. 2. Explain the location of chemoreceptors and their roles. 3. Describe how ADH and aldosterone regulate blood pressure. 4. Explain short-term and long-term regulation of blood pressure.

Neural Controls of Blood Vessels

Most neural controls of blood vessels operate because of reflex arcs, which involve baroreceptors and related afferent fibers. The reflexes are controlled by the car-diovascular center of the medulla in the brain. Their output travels thorough autonomic fibers to the heart and vascular smooth muscle. The neural control mechanism is sometimes influenced by input from chemoreceptors and higher brain centers.

Sympathetic efferents known as vasomotor fibers are used to transmit highly steady impulses from the vasomotor center, which controls blood vessel ­diameter. Nerves arising from the vasomotor center of the medulla oblongata change, in cycles, the diameter­ of the lumen of each blood vessel, controlling the volume of blood that is contained. Vasomotor fibers emerge from the T1 through the L2 levels of the ­spinal cord and innervate the smooth muscle of primarily arterioles but also of other blood vessels. This means the arterioles are nearly always slightly contracted. This is known as vasomotor tone, which is different between various body organs. For example, vasomotor impulses are more frequent in the skin and digestive viscera arterioles but less frequent in the skeletal mus-cles. As a result, they have more constriction than in the skeletal muscles. Generalized vasoconstriction and increased blood pressure result from any increase in sympathetic activity. Vascular muscle can relax slightly because of decreased sympathetic activity. This allows blood pressure to reduce to basal levels. There are three ways that cardiovascular center activity is modified:

From baroreceptors, which respond to arterial pressure changes and stretching

From chemoreceptors, which respond to changes in carbon dioxide, hydrogen, and oxygen levels inthe blood

From the higher brain centers

Baroreceptor Reflexes

Baroreceptors are activated by increased arterialblood pressure and are located in the carotid sinuses, which provide the brain’s major blood supply; in the aortic arch; and in the walls of most large neck and thoracic arteries. Stretching causes the baroreceptors to send impulses quickly to the cardiovascular center. This inhibits the cardioacceleratory and vasomotor centers while stimulating the cardioinhibitor center. Blood pressure decreases as a result of these actions. Baroreceptors are also found in the aortic sinuses of the ascending aorta of the heart and wall of the right atrium. Atrial baroreceptors monitor blood pressure at the vena cava and right atrium, which constitute the end of the systemic circuit. The atrial reflex responds to stretching of the wall of the right atrium.

The circulation is buffered from acute changes in blood pressure by the quick responses of the barore-ceptors. Primarily in the head, blood pressure falls as we stand up after lying down. The blood supply to the brain is protected by the baroreceptors and their actions in the carotid sinus reflex. The baro-receptors that are activated in the aortic reflex help ­balance blood pressure in the overall systemic circuit. Sustained pressure changes, such as chronic hyper-tension, usually override the effects of baroreceptors. The baroreceptors become adapted to monitor pres-sure changes at the new, higher “set point.”

Chemoreceptor Reflexes

Chemoreceptors in theaortic archand carotid arter-ies send impulses to the cardioacceleratory center, increasing cardiac output. They also send impulses to the vasomotor center, causing reflex vasoconstriction. Chemoreceptors act with chemoreceptor reflexes when carbon dioxide levels rise, pH falls, or blood oxygen levels drop quickly. The resultant blood pres-sure increase causes blood to return to the heart and lungs more quickly. The carotid and aortic bodies close to the baroreceptors of the carotid sinuses and aortic arch are the most important chemoreceptors. They play a greater role in regulating respiratory rate, how-ever, than blood pressure.

High Brain Center Influences

The brain stem’s medulla oblongata integrates reflexes that maintain blood pressure. The cerebral cortex and hypothalamus have the ability to change arterial pressure by using relays to the centers of the medulla oblongata. The fight-or-flight response is an example. It is controlled by the hypothalamus, with large effects on blood pressure. Redistribution of blood flow and other cardiovascular responses is also regulated by the hypothalamus. Examples of this redistribution include during body temperature changes and exercise.

Short-Term Regulation by Hormonal Controls

Hormonal controls help to control blood pressure in short-term peripheral resistance changes as well as long-term blood volume changes. Local chemicals known as paracrines help to bring adequate blood flow to servecertain tissues’ metabolic needs. Rarely, large releases of paracrines can affect blood pressure. Short-term hor-monal controls involve antidiuretic hormone (ADH), angiotensin II, atrial natriuretic peptide (ANP), eryth-ropoietin, and the hormones of the adrenal medulla.

Antidiuretic Hormone

Antidiuretic hormone (ADH) is also calledvasopressin.It is produced by the hypothalamus, and released from the posterior lobe of the pituitary gland, due to a decrease in blood volume. It may also be caused by an increase in plasma osmotic concentration, or a secondary increase in circulating angiotensin II. Antidiuretic hormone stimulates the kidneys to conserve water. Although not usually important for regulation of blood pressure on a short-term basis, if blood pressure falls to extremely low levels, its release is greatly increased. Severe hemorrhage is an example of a situation that triggers this release. ADH then helps to restore arterial blood pressure via extensive peripheral vasoconstriction.

Angiotensin II

Angiotensin II is generated within the specialized jux-taglomerular cells of the kidneys, by the enzymaticactions of renin. The kidneys release renin when blood pressure or volume is low.

The steps of the effects of renin are as follows:

Renin converts the liver-produced plasma protein called angiotensinogen to angiotensin I.

In the lung capillaries, angiotensin-converting enzyme (ACE) modifies angiotensin I to angiotensin II, which is an active hormone that has many effects.

Angiotensin II has four important functions, as follows:

It stimulates adrenal production of aldosterone.This causes sodium retention and potassium loss by the kidneys.

It stimulates secretion of ADH. This then stimulates water reabsorption by the kidneys and complements the effects of aldosterone.

It stimulates thirst. This results in increased fluid consumption. The presence of ADH and aldosterone means that the additional consumed water is retained, and blood volume is elevated.

It stimulates cardiac output and causes arteriole constriction. This elevates systemic blood pressure. Angiotensin II has four to eight times the effect on blood pressure than norepinephrine.

Atrial Natriuretic Peptide

Atrial natriuretic peptide (ANP) is produced by the right atrium of the heart. It helps to reduce blood pressure and volume. ANP is produced in response to excessive stretching during diastole. It acts by antago-nizing aldosterone, causing the kidneys to excrete more water and sodium. This reduces blood volume and also results in generalized vasodilation. Ventricular muscle cells, exposed to similar stimuli, produce a related hor-mone known as brain natriuretic peptide (BNP). Both ANP and BNP reduce blood volume and pressure. They accomplish this task in the following ways:

■■ By increasing sodium ion excretion from the kidneys

■■ By promoting water loss from increasing the volume of urine produced

■■ By reducing thirst

■■ By blocking release of ADH, aldosterone,epinephrine, and norepinephrine

■■ By stimulating peripheral vasodilation

When blood volume and pressure decline, the stress on the heart walls is removed. Therefore, ­production of natriuretic peptide stops.

Adrenal Medulla Hormones

Adrenal medulla hormones include epinephrine andnorepinephrine, which are released by the adrenal gland during times of stress. In the blood these hor-mones increase cardiac output and promote generalized vasoconstriction, enhancing the sympathetic response. ­Generally, sympathetic stimulation, which releases epinephrine, causes vasoconstriction and therefore increased blood pressure. However, the parasympa-thetic nervous system has the opposite effect and gen-erally causes vasodilation and decreased blood pressure.


It stimulates adrenal production of aldosterone. This causes sodium retention and potassium loss by the kidneys.when blood pressure falls, or when the blood’s oxygen content becomes abnormally low. It acts directly on the blood vessels. Vasoconstriction increases blood pressure. The production and matura-tion of red blood cells is also stimulated by EPO. These cells increase blood volume and viscosity. They also improve its capacity to carry oxygen.

Long-Term Regulation by Renal Controls

Long-term control of blood pressure involves the kid-neys. This alters blood volume instead of peripheral resistance and cardiac output. There are two mecha-nisms: direct and indirect.

Direct Renal Mechanism

The direct renal mechanism changes blood volume without using hormones. The rate of fluid filtering from the bloodstream to the kidney tubules becomes faster when either blood pressure or blood volume rises. When this occurs, more fluid leaves the body in urine because the kidneys cannot reabsorb the fil-trate quickly enough. Therefore, both blood pressure and volume are lowered. When they are low, water is conserved. It is returned to the bloodstream, and the blood pressure increases.

Indirect Renal Mechanism

The indirect renal mechanism uses the renin-­ angiotensin-aldosterone mechanism. Renin is an enzyme that is released by certain kidney cells into the blood when arterial blood pressure declines. It causes enzymatic claving of angiotensinogen, which is a plasma protein manufactured by the liver. Renin converts­ angiotensinogen to angiotensin I. Then, angiotensin-converting enzyme converts ­angiotensin Ito angiotensin II. The activity of angiotensin-converting enzyme is linked with the capillary ­endothelium pri-marily in the lungs but also in other body tissues.

There are four ways in which angiotensin II sta-bilizes extracellular fluid volume and arterial blood pressure:

Angiotensin II stimulates the adrenal cortex to secrete aldosterone. This hormone enhances renal absorption of sodium. Sodium moves into the bloodstream, followed by water, conserving blood volume. Angiotensin II also directly stimu-lates the kidneys’ reabsorption of sodium.

Angiotensin II causes the posterior pituitary to release ADH. This promotes additional water reabsorption by the kidneys.

Angiotensin II increases the thirst sensation via activation of the hypothalamic thirst center. Water consumption therefore increases, restoring blood volume and blood pressure.

Angiotensin II is a very potent vasoconstrictor. It increases peripheral resistance, which increases blood pressure.

Homeostatic Imbalances

Homeostatic imbalances in blood pressure involve hypertension and hypotension. Hypertension is chronically elevated blood pressure, defined as a sus-tained increase in either systolic pressure or diastolic pressure. In hypertension, systolic pressure is usually above 140 mm Hg and diastolic pressure is usually above 90 mm Hg. Chronic hypertension is common and dangerous because the heart must pump harder against greater resistance, causing the myocardium to enlarge. Nearly 90% of hypertensive patients have primary or essential hypertension, which has no iden-tified, underlying cause. Primary hypertension may be linked to heredity, diet, obesity, age, diabetes mellitus, stress, and smoking. It can usually be con-trolled but cannot be cured. Secondary hypertension is from an identifiable condition such as kidney dis-ease, renal artery obstruction, hyperthyroidism, or Cushing’s syndrome.

Hypotension, defined as blood pressure below90/60 mm Hg, is often linked simply to old age. It is usually only dangerous if it leads to dizziness or faint-ing and, when acute, is an important sign of circu-latory shock. Orthostatic hypotension is a temporary blood pressure drop, which causes dizziness, when a person stands up suddenly after sitting or lying down. It is most common in the elderly. Chronic hypotension may be linked to a more serious disorder such as Addi-son’s disease, hypothyroidism, or severe malnutrition.

1. Describe baroreceptor reflexes that control blood pressure changes.

2. Explain the location of chemoreceptors and their roles.

3. Describe how ADH and aldosterone regulate blood pressure.

4. Explain short-term and long-term regulation of blood pressure.

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