BLOOD PRESSURE The pressure exerted by the blood on vessel wall is known as blood pressure. SYSTOLIC BLOOD PRESSURE The maximum pressure exerted in the arteries during systole of heart. Normal systolic pressure: 120 mm Hg. DIASTOLIC BLOOD PRESSURE The minimum pressure exerted in the arteries during diastole of heart. Normal diastolic pressure: 80 mm Hg. PULSE PRESSURE The difference between the systolic pressure and diastolic pressure. Normal pulse pressure: 40 mm Hg (120 – 80 = 40). MEAN ARTERIAL BLOOD PRESSURE The average pressure existing in the arteries. Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure Pulse Pressure = (Systolic – Diastolic) Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)

1. Regulation of Arterial
Blood Pressure
Maryam Fida (o-1827)
Source: The Guyton and Hall Physiology

2. Definitions
 BLOOD PRESSURE
 The pressure exerted by the blood
on vessel wall is known as blood
pressure.
 SYSTOLIC BLOOD PRESSURE
 The maximum pressure exerted in
the arteries during systole of heart.
 Normal systolic pressure: 120 mm
Hg.
 DIASTOLIC BLOOD PRESSURE
 The minimum pressure exerted in
the arteries during diastole of
heart.
 Normal diastolic pressure: 80 mm
Hg.
 PULSE PRESSURE
 The difference between the systolic
pressure and diastolic pressure.
 Normal pulse pressure: 40 mm Hg
(120 – 80 = 40).
 MEAN ARTERIAL BLOOD PRESSURE
 The average pressure existing in the
arteries.
 Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure
 Pulse Pressure = (Systolic – Diastolic)
 Mean Arterial Blood Pressure
=Diastolic Pressure+1/3(Systolic –
Diastolic)

3. Blood Pressure
Blood Pressure = Cardiac Output X Peripheral Resistance
Blood Pressure =
(Stroke Volume X Heart rate) X Peripheral Resistance
Factors which effect Stroke Volume, Heart rate and Peripheral Resistance ultimately effects
Blood Pressure

4. Regulation of Blood Pressure
 Short Term Regulation
 Long Term Regulation

5. Short Term Regulation of Blood Pressure
 Nervous Mechanisms
 Baroreceptor Reflex
 CNS Ischemic Response
 Cushing’s Reflex / Cushing’s Reaction
 Chemoreceptors
 Hormonal Mechanisms
 Catecholamines
 Renin Angiotensin system
 Vasopressin / ADH
 Miscellaneous Mechanisms
 Capillary Fluid Shift
 Stress Relaxation and reverse stress relaxation

6. Nervous Mechanism
• 1. Baroreceptor Reflex
 Becomes activated within few seconds.
 Baroreceptors are the stretch
receptors in the walls of the carotid
arteries and arch of aorta
 Impulses are carried from these
receptors by hering’s nerve and vagi to
the vasomotor centre in brain stem
which consists of three parts i.e.
 Vasoconstrictor
 Vasodilator
 Sensory part
 Lateral and medial parts: Lateral
part increases heart rate and
medial part decreases heart rate.
 Baroreceptors remain stimulated when mean blood pressure is between 60 -180 mm of hg, however fopr carotid above range is
210. If blood pressure falls below 60 or above 210 or 180 baroreceptor don’t remain active.
 Baroreceptors remain stimulated when mean blood pressure is between 60 -180 mm of hg, however fopr carotid above range is
210. If blood pressure falls below 60 or above 210 or 180 baroreceptor don’t remain acti
 Baroreceptors remain stimulated when mean blood pressure is between 60 -180 mm of hg, however fopr carotid above range is
210. If blood pressure falls below 60 or above 210 or 180 baroreceptor don’t remain activ
 When blood pressure rises above normal,
baroreceptors are stretched more than
normal sending more impulses to the
vasomotor center and bringing back the
blood pressure.
 When there is fall in the blood pressure
below normal, stretch of receptors
decreases so the discharge of impulses
decreases and this decrease discharge
stimulates the vasomotor center, leading
to the rise back of blood pressure.
 As barorecpetors prevent change in blood
pressure, they are known as pressure
buffer system.
 Baroreceptors remain stimulated when
mean blood pressure is between 60 -180
mm of hg, however for carotid above
range is 210. If blood pressure falls below
60 or above 210 or 180 baroreceptor don’t
remain active.

8. 2. CNS Ischemic Response
When mean blood pressure
falls below 60 mm of hg, it
becomes activated
 There is impaired blood flow to the
brain, leading to ischemia of brain
including vasomotor centre.
 Ischemic neurons of vasomotor
centre discharge excessively along
sympathetic pathways leading to
tachycardia and raised blood pressure
 This ischemic response is very
powerful activator of vasomotor
sympathetic system
 This is the last ditch response to
maintain the blood pressure
 Cushing’s Reaction
 Specialized CNS ischemic response
 It is initiated when there is high
intracranial pressure.
 Raised intracranial pressure compresses the
cerebral blood vessels leading to ischemia
of brain causing stimulation of CNS
ischemic response.
 As a result, blood pressure rises which
restores the blood flow to the brain.
 So it’s a protective mechanism.
 In case of ischemic stroke, don’t lower the
blood pressure.
 Average CSF pressure is 12 cm of H20.
Cushing’s reflex is activated when
intracranial pressure rises up to 45 cm of
H20.

9. Chemoreceptors
• These are present in aortic bodies and
carotid bodies
• These are important when blood pressure falls
to very low i.e. up to 50 mm of Hg.
• At this pressure there is increased PCO2,
increased H+ ions and Decreased P02, which
stimulates the peripheral chemoreceptors.
• Impulses are carried along glossopharyngeal
and vagi to vasomotor centre bringing back
the blood pressure.

10. Hormonal Mechanisms
Catecholamines
When blood pressure falls,
there is sympathetic
stimulation and as a
part of this stimulation
large amounts of
catecholamines are
released from adrenal
medulla, they remain in
system for few minutes
exerting the same
effect as the direct
effect of nervous
stimulation.
 VASOPRESSIN/ADH
• It causes vasoconstriction, so as
vasopressin it is involved in short
term regulation.
• ADH is also involved in long term
regulation.

11. Miscellaneous Mechanisms
 Capillary Fluid Shift
 When blood pressure increases,
there is increased capillary
hydrostatic pressure leading to
increase in the filtration of fluid
into interstitial space causing
decreased blood pressure
 This again causes less filtration
from capillaries and so blood
volume increases and this will
try to bring back the blood
pressure.
 Stress relaxation and reverse
stress relaxation
• When blood pressure increases due to
increased blood volume, the smooth
muscle in the vessel wall undergoes
relaxation to accommodate the
increased blood volume without rise in
blood pressure. (Stress Relaxation)
• When blood pressure falls due to blood
loss, the smooth muscle in the vessel
wall contracts around the decreased
blood volume so that decreased blood
volume can adequately fill the blood
vessel. (Reverse stress relaxation)
• This is one of the mechanisms which
prevents the development of
circulatory shock.

12. Long Term Regulation of B.P
 Long term regulation
maintains the blood
pressure for days,
weeks, months and
years.
 It is through renal body
fluid pressure control
systems
The renal body fluid pressure control
system is assisted by 4
mechanisms:
1.. Renin angiotensin mechanism
2.. ADH mechanism
3.. Aldosterone mechanism
4.. Sympathetic impulses to kidney

13. 1. Renin Angiotensin System
• whenever blood pressure falls to low
value:
renal blood flow decreases
GFR decreases
Concentration of NaCl at macula densa
decreases.
This causes release of renin.
Sympathetic stimulation also causes renin
release.
Renin once released remains in system for 1
hour.

14. Rennin acts on Angiotensinogen (which is
formed in liver) and converts it into
angiotensin - I
Angiotensin-I (decapeptide) goes to lungs
where Angiotensin Converting Enzyme converts
it into Angiotensin-II in lungs which is a octa
peptide.
A small amount of angiotensin 3 is also
formed which is not physiologically active.
Angiotensin-II once formed remains in blood
for 2 to 3 minutes.

15. Angiotensin-II exerts different effects i.e.
Vasoconstriction (Short term Regulation)
It acts on adrenal cortex to release aldosterone.
(Long term regulation)
It acts on hypothalamus to stimulate thirst centre.
(Long term regulation)
It also causes release of ADH from hypothalamo
neurohypop[hyseal system. (Long term regulation)
It also causes release of norepinephrine from the
sympathetic post ganglionic nerve endings. (Long
term regulation)
 So we can say that hormonal mechanism is involved in both short term and long term
regulation. It becomes activated in about 20 minutes

17. 2. SYMPATHETIC IMPULSES TO KIDNEY:
 Whenever the blood pressure falls, there is increased
sympathetic discharge which leads to renal
vasoconstriction causing retention of salt and water.

18.  ADH MECHANISM:
 When blood pressure falls there is release of ADH, which
causes water reabsorption from the distal part of renal
tubules.
 ALDOSTERONE MECHANISM:

 SO all the four mechanisms causes salt and water
retention.

 When blood pressure increases above normal all of the
above mechanisms are reversed.