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Blood Pressure Regulation
Nyunt Wai
What is B.P.?

Pressure = force/unit area
Blood pressure =

pressure exerted by blood
on the walls of the

heart or
blood vessels

2
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
More blood

GREATER PRESSURE

Since the arterial system is not very distensible
Arterial BLOOD VOLUME

∞ Arterial BLOOD

PRESSURE
4
GREATER PRESSURE

LESSER PRESSURE

PRESSURE creates FLOW

PRESSURE

∞

FLOW
5
6
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

7
The determinants of BP

blood pressure ∞ cardiac output
8
Blood pressure

∞ Total Peripheral Resistance(TPR)
9
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.?
10
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 ?

11
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

12
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
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.
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
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

16
Regulation of

17
Systemic arterial blood pressure
Total peripheral
= Cardiac output x resistance
(arteriolar tone)

More immediate
More efficient:
RESISTANCE =

1
Radius 4

More economical
18
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

19
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
20
• Kidney: activation of RAA system
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)
21
How does sympathetic N.S. activity
increase BP?
• Direct cardiovascular effects
• Neuroendocrine effects: activation of
– adrenal medulla
– renin-angiotensin-aldosterone (RAA) system

22
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

23
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

24
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
25
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
26
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

27
Renal reabsorption of Water
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
28
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

29
Arterial baroreceptors

30
How the baroreceptor reflex works

Basic network

31
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
32
Carotid sinus, aortic arch

Parasym. fibres in IX and
X cranial nerves

Inhibits VMC

stimulates motor vagal
nuclei

33
•Hypothalamus

•Posterior pituitary

•Vasopressin (ADH)

•Adrenal
medulla

•RAA system

34
HYPOTHALAMUS

VASOPRESSIN

POSTERIOR
PITUITARY

Generalized vasoconstriction

(V1 receptors)

TPR

Renal reabsorption of water

BP

(V2 receptors)
plasma volume

CARDIAC OUTPUT

35
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
36
SENSITIVITY

BARORECEPTORS

CHEMORECEPTORS

50

110 mm Hg

MEAN ARTERIAL B.P.
37
Neural regulation of B.P.
120

Baroreceptor reflex
100
B.P.
mmHg
80

60

40

Chemoreceptor reflex
CNS ischaemic
response
38
The chemoreceptor reflex

39
ARTERIAL
CHEMORECEPTORS

CAROTID BODIES

AORTIC BODIES

40
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
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

42
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

43
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
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.
45
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
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
47
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
Anuria

49
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
50
higher is the BP
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
51

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Blood pressure regulation 2013

  • 2. What is B.P.? Pressure = force/unit area Blood pressure = pressure exerted by blood on the walls of the heart or blood vessels 2
  • 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 4
  • 5. GREATER PRESSURE LESSER PRESSURE PRESSURE creates FLOW PRESSURE ∞ FLOW 5
  • 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 7
  • 8. The determinants of BP blood pressure ∞ cardiac output 8
  • 9. Blood pressure ∞ Total Peripheral Resistance(TPR) 9
  • 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.? 10
  • 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 ? 11
  • 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 12
  • 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 16
  • 18. Systemic arterial blood pressure Total peripheral = Cardiac output x resistance (arteriolar tone) More immediate More efficient: RESISTANCE = 1 Radius 4 More economical 18
  • 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 19
  • 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 20 • 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) 21
  • 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 23
  • 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 24
  • 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 25
  • 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 26
  • 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 27 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 28
  • 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 29
  • 31. How the baroreceptor reflex works Basic network 31
  • 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 32
  • 33. Carotid sinus, aortic arch Parasym. fibres in IX and X cranial nerves Inhibits VMC stimulates motor vagal nuclei 33
  • 35. HYPOTHALAMUS VASOPRESSIN POSTERIOR PITUITARY Generalized vasoconstriction (V1 receptors) TPR Renal reabsorption of water BP (V2 receptors) plasma volume CARDIAC OUTPUT 35
  • 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 36
  • 38. Neural regulation of B.P. 120 Baroreceptor reflex 100 B.P. mmHg 80 60 40 Chemoreceptor reflex CNS ischaemic response 38
  • 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 42
  • 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 43
  • 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. 45
  • 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 47
  • 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
  • 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 50 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 51