Control of blood pressure

Outline
• Short term control (baroreceptors)
– Location
– Types of baroreceptor
– Baroreceptor reflex
• Other stretch receptors
• Long-term control
– Renin/ angiotensin/ aldosterone system
– Vasopressin
– Atrial natiuretic peptide
• Response to blood loss (shock)
 Control of blood pressure
• Mean blood pressure is controlled by changing
total peripheral resistance and or cardiac output.
P = CO x TPR (compare Ohm’s law)

– Cardiac output is controlled by sympathetic and para

sympathetic nerves which effect:
• heart rate
• force of contraction

– TPR controlled by nervous and chemical means to

effect constriction/dilatation of
• arterioles and venules
 Regulation of blood pressure

How is pressure “measured”?

• Short term
– Baroreceptors
• Long term
– Kidney via renin angiotensin system
 Location of
baroreceptors
• Baroreceptors sense stretch and
rate of stretch by generating
action potentials (voltage spikes)

• Located in highly distensible

regions of the circulation to
maximise sensitivity

http://www.cvphysiology.com/Blood Pressure/bp012 baroreceptor anat.gif

 Baroreceptor output
(from single fibres)

Rapid increase in mean pressure Rapid decrease in mean pressure

Response to pulse pressure

From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)
 Two types of baroreceptor

• Type A
– High sensitivity
– High firing rate
• Type C
– Lower sensitivity
– Lower firing rate
– Higher threshold (before firing starts)
• Therefore can deal with higher pressures than
type A which become “saturated”
From “An Introduction to Cardiovascular Physiology”
J.R. Levick
 Response of single baroreceptor
fibre to change in pressure

From “An Introduction to Cardiovascular Physiology” J.R. Levick

 Baroreceptor reflex
Blood pressure falls

Sensors Aortic arch Carotid sinus

Neural integration Nucleus tractus solitarius

Vasoconstriction Cardiac stimulation Cardiac inhibition

Effectors Constriction of veins Increased stroke Increased heart

& arterioles volume rate

Increased peripheral Increased cardiac

resistance output

Increased blood
pressure
Baroreceptor reflex is a
feedback loop
Example: central heating system
Set temperature

Read
temperature

Is temperature
Yes
too high?

No

Boiler on

Negative feedback
Baroreceptor reflex is a
feedback loop
“Read”
pressure

Is pressure
No Yes
too high?

Reduce CO Increase CO

Reduce TPR Increase TPR

Two way negative feedback

Positive feedback loop
Unstable
Set temperature

Read
temperature

Is temperature
No
too high?

Ye
Yes
s

Boiler on

Positive feedback
 Other stretch receptors

• Coronary artery baroreceptors

– Respond to arterial pressure but more sensitive than
carotid and aortic ones

• Veno-atrial mechanoreceptors
– Respond to changes in central blood volume
• Lie down, lift your legs and cause peripheral vasodilatation

• Unmyelinated mechanoreceptors
– Respond to distension of heart
• Ventricular ones during systole; atrial ones during inspiration
Location of receptors in and near the heart
Nucleus tractus solitarius

Cardiac vagal afferents Cardiac pain

myelinated unmyelinated

Spinal cord

Baroreceptors in
coronary arteries and Sympathetic afferents &
aortic arch unmyelinated nociceptors

From “An Introduction to Cardiovascular Physiology” J.R. Levick

 Other receptors
• Heart chemosensors
– Cause pain in response to ischaemia
• K+, lactic acid, bradykinin, prostaglandins
• Arterial chemosensors
– Stimulated in response to
• Hypoxaemia, hypercapnia*, acidosis,
hyperkalaemia**
• Regulate breathing
• Lung stretch receptors
– Cause tachycardia during inspiration
*too much CO2
**too much K+
Overview of short-term control mechanisms

From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)
 Long term control of blood pressure

• Involves control of blood volume/sodium

balance by the kidneys
– Hormonal control
• Renin-angiotensin-aldosterone system
• Antidiuretic hormone (vasopressin)
• Atrial natiuretic peptide
– Pressure natriuresis
 Renin/angiotensin/
Reduced renal
blood flow
aldosterone system
Increased
Juxtaglomerular blood volume
apparatus LV filling pressure)

Increased
Renin Fluid re-absorption pre-load

(LV pressure
Angiotensinogen Sodium retention
beginning of systole)

Increased
after-load
Angiotensin I
Increased aldosterone
Angiotensin II secretion

Veins
vasoconstriction
Arteries
 Vasopressin
• Enhances water retention
• Causes vasoconstriction
• Secretion increased by unloading of
aortic Baroreceptors and atrial sensors

http://www.cvphysiology.com/Blood%20Pressure/BP016.htm
 Atrial natiuretic peptide

• Increases salt excretion via kidneys

– By reducing water reabsorption in the
collecting ducts
– relaxes renal arterioles
– inhibits sodium reabsorption in the
distal tubule

• Released in response to stimulation of

atrial receptors
Summary of long term BP control
• Cardiac output and BP depend on renal control of
extra-cellular fluid volume via:
– Pressure natriuresis, (increased renal filtration)
– Changes in:
• Vasopressin
• Aldosterone
• Atrial natiuretic peptide

All under the control of altered cardiovascular

receptor signaling
 Shock
Definition:
A pathophysiological disorder characterised by acute
failure of the cardiovascular system to perfuse the
tissues of the body adequately.
Levick J.R. “An Introduction to Cardiovascular Physiology”

Symptoms
– Cold, clammy skin
– Muscular weakness
– Rapid and shallow breathing
– Rapid and weak pulse
– Low pulse pressure (and sometimes mean pressure)
– Reduced urine output
– Confusion
 Types of shock
– Hypovolaemia
• Caused by drop in blood (plasma) volume
– e.g. haemorrhage, diarrhoea, vomiting, injury
– Septic
• Caused by bacterial endotoxins
– e.g. salmonella
– Cardiogenic
• An acute interruption of of cardiac function
– e.g. myocarditis (inflammation of the heart muscle) or
myocardial infarction
– Anaphylactic
• Caused by allergic reaction
 Effect of blood loss

• less than 10%, no serious symptoms

– e.g. blood transfusion
• 20 - 30% blood loss not usually life
threatening
• greater than 30%, severe drop in BP
and, often, death due to impaired
cerebral and coronary perfusion
Response to moderate blood loss
(compensated haemorrhage)

• Blood volume falls therefore pulse pressure

and stroke volume fall. (Frank-Starling
mechanism: reduced LV contractile force)
• Cardiopulmonary stretch receptor and
baroreceptor activity falls
• Arterial chemoreceptor activity increases, due
to hypoxia and acidosis
 rapid breathing
 release of vasoconstrictors
Vasopressin, angiotensin etc.
Response to moderate blood loss

More serious blood loss

can be treated by
transfusion to lessen the
effects shown here
 Uncompensated shock

If compensation is not sufficient, organ

failure occurs due to inadequate perfusion
• Heart
• Kidney
• Brain