Control of Blood Pressure

Changes in blood pressure are routinely made in order to direct appropriate amounts of oxygen
and nutrients to specific parts of the body. For example, when exercise demands additional
supplies of oxygen to skeletal muscles, blood delivery to these muscles increases, while blood
delivery to the digestive organs decreases. Adjustments in blood pressure are also required when
forces are applied to your body, such as when starting or stopping in an elevator.

Blood pressure can be adjusted by producing changes in the following variables:

 Cardiac output can be altered by changing stroke volume or heart rate.

 Resistance to blood flow in the blood vessels is most often altered by changing the
diameter of the vessels (vasodilation or vasoconstriction). Changes in blood viscosity
(its ability to flow) or in the length of the blood vessels (which increases with weight
gain) can also alter resistance to blood flow.

The following mechanisms help regulate blood pressure:

 The cardiovascular center provides a rapid, neural mechanism for the regulation of
blood pressure by managing cardiac output or by adjusting blood vessel diameter. Located in the
medulla oblongata of the brain stem, it consists of three distinct regions:
o The cardiac center stimulates cardiac output by increasing heart rate and
contractility. These nerve impulses are transmitted over sympathetic cardiac
nerves.
o The cardiac center inhibits cardiac output by decreasing heart rate. These nerve
impulses are transmitted over parasympathetic vagus nerves.
o The vasomotor center regulates blood vessel diameter. Nerve impulses
transmitted over sympathetic motor neurons called vasomotor nerves innervate
smooth muscles in arterioles throughout the body to maintain vasomotor tone, a
steady state of vasoconstriction appropriate to the region.
 The cardiovascular center receives information about the state of the body through the
following sources:
o Baroreceptors are sensory neurons that monitor arterial blood pressure. Major
baroreceptors are located in the carotid sinus (an enlarged area of the carotid
artery just above its separation from the aorta), the aortic arch, and the right
atrium.
o Chemoreceptors are sensory neurons that monitor levels of CO 2 and O 2. These
neurons alert the cardiovascular center when levels of O 2 drop or levels of
CO 2 rise (which result in a drop in pH). Chemoreceptors are found in carotid
bodies and aortic bodies located near the carotid sinus and aortic arch.
o Higher brain regions, such as the cerebral cortex, hypothalamus, and limbic
system, signal the cardiovascular center when conditions (stress, fight‐or‐flight
response, hot or cold temperature) require adjustments to the blood pressure.
 The kidneys provide a hormonal mechanism for the regulation of blood pressure by
managing blood volume.
 o The renin‐angiotensin‐aldosterone system of the kidneys regulates blood
volume. In response to rising blood pressure, the juxtaglomerular cells in the
kidneys secrete renin into the blood. Renin converts the plasma protein
angiotensinogen to angiotensin I, which in turn is converted to angiotensin II
by enzymes from the lungs. Angiotensin II activates two mechanisms that raise
blood pressure:
 Angiotensin II constricts blood vessels throughout the body (raising
blood pressure by increasing resistance to blood flow). Constricted blood
vessels reduce the amount of blood delivered to the kidneys, which
decreases the kidneys' potential to excrete water (raising blood pressure by
increasing blood volume).
 Angiotensin II stimulates the adrenal cortex to secrete aldosterone, a
hormone that reduces urine output by increasing retention of H 2O and
Na + by the kidneys (raising blood pressure by increasing blood volume).

Various substances influence blood pressure. Some important examples

follow:

 Epinephrine and norepinephrine, hormones secreted by the

adrenal medulla, raise blood pressure by increasing heart rate and
the contractility of the heart muscles and by causing
vasoconstriction of arteries and veins. These hormones are secreted
as part of the fight‐or‐flight response.
 Antidiuretic hormone (ADH), a hormone produced by the
hypothalamus and released by the posterior pituitary, raises blood
pressure by stimulating the kidneys to retain H 2O (raising blood
pressure by increasing blood volume).
 Atrial natriuretic peptide (ANP), a hormone secreted by the
atria of the heart, lowers blood pressure by causing vasodilation
and by stimulating the kidneys to excrete more water and
Na +(lowering blood pressure by reducing blood volume).
 Nitric oxide (NO), secreted by endothelial cells, causes
vasodilation.
 Nicotine in tobacco raises blood pressure by stimulating
sympathetic neurons to increase vasoconstriction and by
stimulating the adrenal medulla to increase secretion of
epinephrine and norepinephrine.
 Alcohol lowers blood pressure by inhibiting the vasomotor center
(causing vasodilation) and by inhibiting the release of ADH
(increasing H 2O output, which decreases blood volume).

Blood Pressure
The body’s blood pressure is a measure of the pressures within the cardiovascular system during
the pumping cycle of the heart. It is influenced by a vast number of variables, and can alter in
either direction for various reasons. Everyone’s blood pressure is slightly different and can
change throughout the day depending on activity.

There is a range of normal blood pressures that we consider as acceptable. When blood pressure
is outside of this normal range of values, people can start to have problems in both the long and
short term. Our body tries to maintain a stable blood pressure in the process of homeostasis.

Blood pressure is measured using an automated blood pressure monitor, or manually using a
stethoscope and sphygmomanometer. It is given as two values (eg 120/80 mmHg), measured in
“millimeters of mercury (mmHg)”:

 Systolic pressure – the first number (120 mmHg in the example) is the pressure of the blood
during the heart contraction.
 Diastolic pressure – the second number (80 mmHg in the example) is the pressure of the blood
after one contraction but before the next contraction.

Blood pressure can be calculated as:

Flow x Resistance

Mean arterial blood pressure = cardiac output x total peripheral resistance

Short-Term Regulation of Blood Pressure

Short-term regulation of blood pressure is controlled by the autonomic nervous system.

Changes in blood pressure are detected by baroreceptors. These are located in the arch of the
aorta and the carotid sinus.

 Increased arterial pressure stretches the wall of the blood vessel, triggering the baroreceptors.
These baroreceptors then feedback to the autonomic nervous system. The ANS then acts to
reduce the heart rate and cardiac contractility via the efferent parasympathetic fibres (vagus
nerve) thus reducing blood pressure.
 Decreased arterial pressure is detected by baroreceptors, which then trigger a sympathetic
response. This stimulates an increase in heart rate and cardiac contractility leading to an
increased blood pressure.

Baroreceptors cannot regulate blood pressure long-term. This is because the mechanism of
triggering baroreceptors resets itself once a more adequate blood pressure is restored.

Long-Term Regulation of Blood Pressure

There are several physiological mechanisms that regulate blood pressure in the long-term, the
first of which is the renin-angiotensin-aldosterone system (RAAS).
Renin-Angiotensin-Aldosterone System (RAAS)

Renin is a peptide hormone released by the granular cells of the juxtaglomerular apparatus in
the kidney. It is released in response to:

 Sympathetic stimulation
 Reduced sodium-chloride delivery to the distal convoluted tubule
 Decreased blood flow to the kidney

Renin facilitates the conversion of angiotensinogen to angiotensin I which is then converted to

angiotensin II using angiotensin-converting enzyme (ACE).

Angiotensin II is a potent vasoconstrictor. It acts directly on the kidney to increase sodium

reabsorption in the proximal convoluted tubule. Sodium is reabsorbed via the sodium-hydrogen
exchanger. Angiotensin II also promotes release of aldosterone.

ACE also breaks down a substance called bradykinin which is a potent vasodilator. Therefore,
the breakdown of bradykinin potentiates the overall constricting effect.

Aldosterone promotes salt and water retention by acting at the distal convoluted tubule to
increase expression of epithelial sodium channels. Furthermore, aldosterone increases the
activity of the basolateral sodium-potassium ATP-ase, thus increasing the electrochemical
gradient for movement of sodium ions.

More sodium collects in the kidney tissue and water then follows by osmosis. This results in
decreased water excretion and therefore increased blood volume and thus blood pressure.

Anti-Diuretic Hormone (ADH)

The second mechanism by which blood pressure is regulated is release of Anti Diuretic
Hormone (ADH) from the OVLT of the hypothalamus in response to thirst or an increased
plasma osmolarity.

ADH acts to increase the permeability of the collecting duct to water by inserting aquaporin
channels (AQP2) into the apical membrane.

It also stimulates sodium reabsorption from the thick ascending limb of the loop of Henle. This
increases water reabsorption thus increasing plasma volume and decreasing osmolarity.

Further Control of Blood Pressure

Other factors that can affect long-term regulation of blood pressure are natriuretic peptides.
These include:

 Atrial natriuretic peptide (ANP) is synthesised and stored in cardiac myocytes. It is released
when the atria are stretched, indicating of high blood pressure.
 ANP acts to promote sodium excretion. It dilates the afferent arteriole of the glomerulus,
increasing blood flow (GFR). Moreover, ANP inhibits sodium reabsorption along the nephron.
Conversely, ANP secretion is low when blood pressure is low.
 Prostaglandins act as local vasodilators to increase GFR and reduce sodium reabsorption. They
also act to prevent excessive vasoconstriction triggered by the sympathetic nervous and renin-
angiotensin-aldosterone system