Handout 1 – 4

4. Review the physiology and regulation of arterial blood pressure

Short-Term Regulation of Blood Pressure

A. Baroreceptor Reflex

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 fibers (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.

B. Chemoreceptor Reflex
It is much like the baroreceptors except that the chemoreceptors initiate the response.
These chemoreceptors are sensitive to low oxygen, carbon dioxide excess and hydrogen ion
excess. They are in the carotid bodies and aortic bodies. However, this reflex is not powerful
until pressure falls below 80 mm Hg. Therefore, this reflex is important at lower pressures to
prevent further decrease in pressure.

C. CNS Ischemic Response

It is one of the most powerful of all the activators of the sympathetic vasoconstrictor
system. It is greatly stimulated at a pressure of 15 to 20 mm Hg. It operates as an emergency
pressure control system which acts to prevent any further decrease in arterial pressure wherein
blood flow to the brain decreases close to a lethal level. This is why it is sometimes called “last-
ditch stand”.

When blood flow to the vasomotor center is greatly decreased causing cerebral
ischemia this excites the vasoconstrictor and cardioaccelerator neurons which rises the systemic
arterial pressure.
Long Term Regulation of Blood Pressure

A. 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.

B. Anti-Diuretic Hormone (ADH)

The second mechanism by which blood pressure is regulated is release of Anti Diuretic Hormone
(ADH) from the osmoreceptors 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.

C. Lower Pressure Receptors

Atrial natriuretic peptide (ANP) is synthesized 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.
Other Vasomotor Reflexes:

A. Atrial stretch receptor reflex- causes dilation of the afferent arterioles in kidneys which increases
the glomerular filtration rate. At the same time transmits signals to hypothalamus to decrease
secretion of antidiuretic hormone (ADH). The results of both combined as increase in filtration
and low water retention lowers blood volume which reduces back to normal the blood pressure.
B. Thermoreceptors – the receptors when exposed to heat causes vasoconstriction and when cold
causes vasodilation.
C. Pulmonary Receptors – when there is increase in pulmonary arterial pressure the low-pressure
receptors on the walls of the pulmonary artery elicits reflexes parallel to baroreceptors to make
total reflex system more potent for control of arterial pressure.

Intermediate Mechanisms:

A. Stress-relaxation mechanism – when pressure in the blood vessels becomes too high, they
become stretched and so they keep on stretching more and more, as a result the pressure falls.

B. Capillary-fluid shift mechanism – when capillary pressure falls, fluid is absorbed from the tissues.
Conversely, when capillary pressure rises too high, fluid is lost into the tissues.

PPT:
Short-Term Regulation of Blood Pressure

A. Baroreceptor Reflexes - sensitive in the range of 60 – 160 mmHg

B. Chemoreceptor Reflexes – responds to increase in PCO2 and H+ concentration, and decrease in
PO2
C. CNS Ischemic Response – “last ditch”

Long-term Regulation of Blood Pressure:

 1. Renin-Angiotensin—Aldosterone System – most important in Na+ retention in order to maintain
the blood volume
2. Anti-diuretic hormone (ADH) – will cause water reabsorption at kidney tubules
3. Low-pressure Volume receptors - Atrial Natriuretic Peptide (ANP) regulates Na+ excretion

Other Vasomotor Reflexes:

A. Atrial stretch receptor reflex

B. Thermoreceptors
C. Pulmonary Receptors