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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
Neural integration
Nucleus tractus solitarius
Vasoconstriction
Effectors
Carotid sinus
Cardiac inhibition
Cardiac stimulation
Constriction of veins
& arterioles
Increased stroke
volume
Increased peripheral
resistance
Increased heart
rate
Increased cardiac
output
Increased blood
pressure
Baroreceptor reflex is a
feedback loop
Example: central heating system
Set temperature
Read
temperature
Yes
Is temperature
too high?
No
Boiler on
Negative feedback
Baroreceptor reflex is a
feedback loop
“Read”
pressure
Is pressure
too high?
No
Yes
Reduce CO
Increase CO
Reduce TPR
Increase TPR
Two way negative feedback
Positive feedback loop
Unstable
Set temperature
Read
temperature
No
Is temperature
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
myelinated
Cardiac pain
unmyelinated
Spinal cord
Baroreceptors in
coronary arteries and
aortic arch
Sympathetic afferents &
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
Reduced renal
blood flow
Juxtaglomerular
apparatus
Renin
Angiotensinogen
Renin/angiotensin/
aldosterone system
Increased
blood volume
LV filling pressure)
Increased
pre-load
Fluid re-absorption
(LV pressure
beginning of systole)
Sodium retention
Increased
after-load
Angiotensin I
Angiotensin II
Increased aldosterone
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