Blood pressure (BP) is the pressure exerted by blood on the walls of the heart and vessels, influenced by cardiac output and total peripheral resistance. Various factors such as age, sex, and physical states affect BP variations, while the sympathetic nervous system and renin-angiotensin-aldosterone system are critical regulators. The baroreceptor reflex provides immediate adjustments for maintaining BP homeostasis in response to blood volume changes.

1. Blood Pressure Regulation
Nyunt Wai

2. What is B.P.?
Pressure = force/unit area
Blood pressure =
pressure exerted by blood
on the walls of the
heart or
blood vessels
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3. Container vs. Content example
same container;
same capacity;
less content
same content;
greater capacity
as the container
expands
PRESSURE falls
PRESSURE falls
e.g. haemorrhage
e.g. generalized
vasodilation
3

4. More blood
GREATER PRESSURE
Since the arterial system is not very distensible
Arterial BLOOD VOLUME
∞ Arterial BLOOD
PRESSURE
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5. GREATER PRESSURE
LESSER PRESSURE
PRESSURE creates FLOW
PRESSURE
∞
FLOW
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6. 6

7. Functions of BP
• Intraventricular BP  ejection of blood (stroke volume)
• Systemic arterial BP  blood flow to tissues (tissue
perfusion)
• Capillary hydrostatic pressure  filtration (tissue fluid
formation)
• Systemic venous BP  blood flow back to the heart
(venous return)
The unconditional term
BLOOD PRESSURE
refers to
SYSTEMIC ARTERIAL
BLOOD PRESSURE
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8. The determinants of BP
blood pressure ∞ cardiac output
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9. Blood pressure
∞ Total Peripheral Resistance(TPR)
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10. Systemic arterial blood pressure
= Cardiac output x Total peripheral
resistance (TPR)
or
Systemic vascular
reistance (SVR)
The 2 Major Determinants of Arterial B.P.
The other Determinants of Arterial B.P.?
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11. Ventricular contraction
Ventricular relaxation
Aorta is the most
elastic artery
When aortic elasticity
decreases (ageing or
disease):
Less expansion during
systole  Incr. SBP
Less elastic recoil
during diastole  decr.
DBP
Pulse pressure ?
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12. The Determinants of Arterial B.P.
SBP
DBP
• SBP
• Aortic distensibility
(elasticity)
• TPR
• Stroke volume
• Aortic distensibility
(elasticity)
SBP = CO x TPR
DBP = CO x TPR
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13. Physiological Variations in BP
• Age:
– SBP and DBP gradually rise with age (after about 30 years), the
SBP more so and more sustained than the DBP
• Sex:
– the rise in BP with age is greater in males
• Circadian variation (diurnal variation):
– lowest during sleep (nocturnal dip) and highest in the mornings after
waking up
• Increased transiently during physical stress (e.g. muscular
exercise), mental stress(anger, apprehension, resentment, mental
concentration), emotional excitement
• The effect of Gravity: When erect, BP in any vessel
varies in relation to the vertical distance from the heart
level

14. Physiological Variations in BP
• Gravity
– In an upright position, BP
in the arteries below the
heart level is increased,
and that in the arteries
above the heart level is
decreased by 0.77 mm Hg
for each cm of vertical
distance below or above
the heart.
– Thus, routine
measurement of BP
should be performed with
the artery at the heart
level.

15. Effect of Gravity
• Pressure in large artery in the
foot 105 cm below the heart =
[0.77 mmHg/cm x 105 cm = 80
mm Hg)] +
• 100 mm Hg (Mean ABP at heart
level)
• = 180 mm Hg
• Pressure in vein in the foot 105
cm below the heart = [0.77
mmHg/cm x 105 cm = 80 mm
Hg)] +
• 4 mm Hg (right atrial pressure)
• = 84 mm Hg

16. REGULATION OF SYSTEMIC ARTERIAL B.P.
– MAINTENANCE OF RESTING B.P.
B.P. HOMEOSTASIS
• SITUATIONAL ADJUSTMENT OF B.P.
e.g. changes in B.P. during muscular exercise
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17. Regulation of
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18. Systemic arterial blood pressure
Total peripheral
= Cardiac output x resistance
(arteriolar tone)
More immediate
More efficient:
RESISTANCE =
1
Radius 4
More economical
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19. BP REGULATORY MECHANISMS
NEURAL: CARDIOVASCULAR REFLEXES
 Baroreceptor reflexes
 Chemoreceptor reflexes
 Brain(CNS) ischaemic response
Short term:
Rapid
Short term:
HORMONAL
Intermediate
 Catecholamines
 Renin-angiotensin-aldosterone(RAA) system
 Vasopressin
Long term
RENAL-BODY FLUID CONTROL SYSTEM
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20. Integrating centres
Afferents
Efferents
Hypothalamus
Vasopressin
Brain stem: Medulla
X
IX, X
(Parasym)
(Parasym)
Spinal cord:
SYMPATHETIC
NERVOUS
SYSTEM
Receptors
• Baroreceptors
• Chemoreceptors
Sym .outflow
Effectors
• Heart, Blood vessels
• Adrenal medulla: Catecholamines
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• Kidney: activation of RAA system

21. Sympathetic Nervous System
•
•
•
•
Major effector system for BP control
Increased sympathetic tone  incr. BP
decreased sympathetic tone  decr. BP
Sym.N.S. is under the control of vasomotor
centre (VMC) in the medulla
• Descending tracts from the VMC excites the
sympathetic nervous system
• Inputs from the broreceptors and other receptors
go to the VMC (the integrating centre)
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22. How does sympathetic N.S. activity
increase BP?
• Direct cardiovascular effects
• Neuroendocrine effects: activation of
– adrenal medulla
– renin-angiotensin-aldosterone (RAA) system
22

23. Sympathetic tone
SYMPATHETIC
OUTFLOW
DIRECT CARDIOVASCULAR EFFECTS
HR
SV
Venoconstrictn
Arteriolar constrictn
Capillary pressure
Venous return
ISF formation
CARDIAC OUTPUT
TPR
Plasma loss
BLOOD PRESSURE
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24. Sympathetic tone
SYMPATHETIC
OUTFLOW
NEUROENDOCRINE EFFECTS
ADRENAL MEDULLA
Secretion of
CATECHOLAMINES
JG CELLS IN KIDNEY
Activation of
RENIN- ANGIOTENSINALDOSTERONE SYSTEM
CARDIOVASCULAR EFFECTS
VOLUME EFFECTS
BLOOD PRESSURE
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25. CATECHOLAMINES
Adrenaline
Noradrenaline
Dopamine
b- receptors
a- receptors
Vasoconstriction
Cardiostimulatory effects:
Automaticity (SANodal
discharge)
Heart Rate
Conductivity
Excitability
Myocardial contractility
TPR
Stroke volume
Cardiac output
BLOOD PRESSURE
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26. RENIN- ANGIOTENSIN-ALDOSTERONE SYSTEM
BLOOD
VOLUME/PRESSURE
Baroreceptor reflex
Sympathetic tone
Renal perfusion pressure
LIVER
Juxtaglomerular(JG) cells in
afferent arteriolar muscle coat in KIDNEY
Angiotensin-
Angiotensinogen
RENIN
Angiotensin I
Converting
Enzyme
ANGIOTENSIN II
VASCULAR and VOLUME EFFECTS
Endothelial cells of
pulmonary circulation
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27. ANGIOTENSIN II
VASOCONTRICTION
Vascular smooth muscle
Sympathetic nerve endings
Brain: Hypothalamus
TPR
Facilitates release of
NORADRENALINE
Release of VASOPRESSIN
Stimulation
of THIRST
Adrenal cortex
Water intake
Secretion of ALDOSTERONE
Renal reabsorption of Sodium
BLOOD VOLUME
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Renal reabsorption of Water

28. THE BARORECEPTOR REFLEX
 operates within seconds
 for moment to moment, day to day control
of BP
 for BP homeostasis in the face of
challenges such as blood loss
 Afferents: Parasympathetic
 Efferents: Sympathetic noradrenergic
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29. Baroreceptors = stretch receptors in the walls of
• Heart
Atria
Volume receptors
Low pressure baroreceptors
• Arteries (arterial baroreceptors)
Aortic arch
High pressure baroreceptors
Carotid sinus
Stimulation of Stretch
receptors in the wall
Stretch on
the wall
BP
Wall
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30. Arterial baroreceptors
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31. How the baroreceptor reflex works
Basic network
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32. Incr. baroreceptor discharge
• Stimulates the Parasympathetic centres
(Dorsal motor nucleus of vagus) in the
medulla
• Inhibits the vasomotor centre (VMC) in the
medulla (through inhibitory interneurones)
– Decr. excitatory discharge from the VMC to
the Sympathetic Nervous System in the spinal
cord
–  decr. sympathetic noradrenergic discharge
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33. Carotid sinus, aortic arch
Parasym. fibres in IX and
X cranial nerves
Inhibits VMC
stimulates motor vagal
nuclei
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34. •Hypothalamus
•Posterior pituitary
•Vasopressin (ADH)
•Adrenal
medulla
•RAA system
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35. HYPOTHALAMUS
VASOPRESSIN
POSTERIOR
PITUITARY
Generalized vasoconstriction
(V1 receptors)
TPR
Renal reabsorption of water
BP
(V2 receptors)
plasma volume
CARDIAC OUTPUT
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36. Note
• BP may not fall with minor haemorrhage
• Fall in venous return is detected by low
pressure baroreceptors  increase in
TPR  compensates for fall in CO  BP
unchnaged
• When blood loss is >20% of circulating
blood volume, the fall in CO is great
enough to cause a fall in BP
• BP = CO x TPR
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37. SENSITIVITY
BARORECEPTORS
CHEMORECEPTORS
50
110 mm Hg
MEAN ARTERIAL B.P.
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38. Neural regulation of B.P.
120
Baroreceptor reflex
100
B.P.
mmHg
80
60
40
Chemoreceptor reflex
CNS ischaemic
response
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39. The chemoreceptor reflex
39

40. ARTERIAL
CHEMORECEPTORS
CAROTID BODIES
AORTIC BODIES
40

41. BP
BLOOD FLOW  STAGNATION
O2 delivery to tissues (stagnant hypoxia)
CO2 uptake from tissues
O2
CO2
(in tissues)
Stimulation of chemoreceptors
IX, X
nerves
•Stimulation of medullary respiratory centre
•Stimulation of medullary VMC
sympathetic discharge
BP

42. The CNS ischaemic response
Medulla oblongata
CEREBRAL
BLOOD FLOW
CNS ISCHAEMIA
PO2
BLOOD
PRESSURE
VASOMOTOR
PCO2
Stagnant
hypoxia
CENTRE
Spinal Cord
(+)
(+)
SYMPATHETIC
OUTFLOW
Sympathetic tone
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43. CUSHING’S
REFLEX
HEAD INJURY
Increased intracranial pressure
Pressure on cerebral arteries
CNS ISCHAEMIA
CEREBRAL
BLOOD FLOW
BLOOD
PRESSURE
Normal
BARORECEPTOR REFLEX
PO2
VMC
PCO2
Stagnant
hypoxia
VAGAL TONE
HEART RATE
(+)
(+)
SYMPATHETIC
OUTFLOW
Sympathetic tone
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44. Head injury CNS ischaemia The rise in BP
• Baroreceptor reflex
–  stimulation of vagus  fall in HR (since
parasympathetic control of HR is dominant
over sympathetic control)
–  but baroreflex-mediated inhibition of VMC
is counterbalanced by direct stimulation of
VMC by CNS ischaemia
–  sympathetic-mediated generalized
vasoconstriction maintained  Incr. in BP
Slow, full and bounding pulse
CUSHING’S REFLEX
44

45. Cushing's reflex
• Because the skull is rigid
after infancy, intracranial
masses or swelling may
increase intracranial
pressure. When intracranial
pressure is increased
sufficiently, regardless of the
cause, Cushing's reflex and
other autonomic
abnormalities can occur.
• Cushing's reflex includes
systolic hypertension,
increased pulse pressure,
and bradycardia.
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46. Renal regulation of B.P.
I. Physical : by variation of Glomerular
filtration pressure  variation in urine
formation
II. Hormonal : by secretion of renin
•  Renin-Angiotensin (AGII)Aldosterone system (RAAS)
46

47. Renal regulation of B.P.
When blood volume and BP is increased,
KIDNEYS excrete excess fluid by
• Pressure diuresis
increased urine formation as a result of increased
glomerular filtration due to raised renal perfusion
pressure
• Pressure natriuresis
increased urinary excretion of sodium as a
result of increased glomerular filtration of
sodium due to raised renal perfusion pressure
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48. Renal regulation of B.P.
When blood volume and BP is decreased:
 decr. glomerular capillary H.P.  decr.GFR 
• Oliguria (deceased urine formation)
• Anuria (renal shutdown – no urine formation)
Thus KIDNEYS conserve ECF Volume
48

49. Anuria
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50. Summary :Systemic Arterial
Blood Pressure
• Varies with the amount of blood in the systemic
arterial system (begins at the aorta, ends at
arterioles in various tissues)
• This is because the systemic arteries are not
very distensible
• The greater the cardiac output, the greater the
inflow of blood into the systemic arterial system,
the higher is the BP
• The greater the TPR, the lesser the outflow of
blood out of the systemic arterial system, the
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higher is the BP

51. Systemic Arterial Blood
Pressure
• Sympathetic nervous system and the RAA
system are powerful systems that can increase
BP
• Moment to moment control is by baroreceptor
reflex.
• What is the use of increasing the BP when blood
supply to almost all tissues are shut down by
arteriolar constriction?
• Ans. Local vasodilatory mechanisms in the vital
organs- the brain and the heart, will overcome
the systemic vasoconstrictor effect– diverting
blood flow to them at the expense of other
organs and tissues
End
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