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REGULATION OF BLOOD PRESSURE
Prof. Sultan Ayoub Meo
MBBS, Ph.D (Pak), M Med Ed (Dundee), FRCP (London),
FRCP (Dublin), FRCP (Glasgow), FRCP (Edinburgh)
Professor and Consultant, Department of Physiology,
College of Medicine, King Saud University, Riyadh, KSA
 Factors regulating arterial blood pressure
 Explain how they influence arterial blood pressure.
 Physiological importance of regulating arterial blood pressure
 Discuss short term, intermediate and long-term regulation of
blood pressure; nervous, hormonal and renal regulation of
arterial blood pressure.
LECTURE OBJECTIVES
REGULATION OF BLOOD PRESSURE
REGULATION OF BLOOD PRESSURE
SHORT TERM REGULATION OF
BLOOD PRESSURE
1. Baroreceptors Reflex Mechanism
2. Chemoreceptors Mechanism
3. CNS Ischemic Response Mechanism
4. Atrial Stretch Volume Receptors
Rapidly acting within seconds to minutes
1. THE BARORECEPTORS
Changes in MAP are detected by
baroreceptors (pressure receptors) in the
carotid and aortic arteries.
Carotid baroreceptors are located in the
carotid sinus, both sides of the neck.
Aortic baroreceptors are located in the
aortic arch.
These receptors provide information to
the cardiovascular centres in the medulla
oblongata about the degree of stretch
with pressure changes.
Guyton and Hall, pp 174
1. THE BARORECEPTORS
 At normal arterial pressure the
baroreceptors are active.
 Increased blood pressure increases
their rate of activity, while
decreased pressure decreases the
rate of firing (activity).
 They play an important role in
maintaining relatively constant
blood flow to vital organs such as
brain during rapid changes in
pressure such as standing up after
lying down. That is why they are
called “pressure buffers”.
1. THE BARORECEPTORS
1. THE BARORECEPTORS
↑ MAP
Baroreceptors
↑ Parasympathetic
(vagal) activity
↓ Sympathetic
activity
↓ HR ↓ SV ↓ TPR ↓ MAP
1. THE BARORECEPTORS
↓ MAP
Baroreceptors
↓ Parasympathetic
(vagal) activity
↑ Sympathetic
activity
↑ HR ↑ SV ↑ TPR  MAP
1. THE BARORECEPTORS
1. THE BARORECEPTORS
 Baroreceptors are important in maintaining MAP constant
during changes in body posture.
 When change of posture from supine to erect, drop in the
MAP in the head and upper part of the body.
 The barorecptor reflex is activated → strong sympathetic
impulses → vasoconstriction. This minimizes the drop in
MAP.
1. THE BARORECEPTORS
ARTERIAL BARORECEPTOR REFLEX
ROLE IN HEMORRAHAGE
2. THE CHEMORECEPTOR REFLEX
 Chemoreceptors have high blood flow
(1200 ml/min/g tissue). This makes it easy
for these cells to detect changes in O2, CO2,
and H+.
 Reduced blood flow (due to reduced MAP)
stimulates the chemoreceptors through
oxygen lack, increased hydrogen ions or
carbon dioxide.
 Chemoreceptors are stimulated when the
MAP is lower than 60 mmHg.
 Response is excitatory, NOT inhibitory;
mainly through activation of sympathetic
nervous system.
 They reduce blood flow to unessential areas
and protect vital tissues like brain and heart.
3. CNS ISCHEMIC RESPONSE
 CNS ischemic response operates rapidly to prevent further
decrease in MAP whenever blood flow to the brain decreases.
 It is one of the most powerful activators of the sympathetic
vasoconstrictor system.
 When MAP < 20 mmHg → cerebral ischemia of vasomotor center
→ strong excitation of vasomotor center (due to accumulation of
CO2, lactic acid,) → strong vasoconstriction of blood vessels
including the kidney arterioles.
4. ATRIAL STRETCH VOLUME RECEPTORS
Receptors in large veins close to heart, walls of the atria (response of blood volume).
An increased blood volume  stretch of atria  activate atrial volume receptors 
sensory afferent nerves to medulla inhibiting the cardiovascular centre  This results
into decreased blood volume through:
(a)   sympathetic drive to kidney:
-  dilate afferent arterioles   glomerular capillary hydrostatic pressure 
GFR   blood volume (towards normal).
-  renin secretion (Renin is an enzyme which activates angiotensinogen in
blood). Inhibition of renin secretion  inhibit RAAS  inhibit aldosterone
production   Blood volume (towards normal)
(b)   ADH secretion   blood volume (towards normal).
(c)   Atrial Natriuretic Peptide (ANP) causes loss of blood volume.
INTERMEDIATE TERM REGULATION OF
BLOOD PRESSURE
1. Renin – Angiotensin system
2. Capillary shift mechanism
3. Stretch relaxation of vessels
Respond from 30 min to several hrs
1. Renin – Angiotensin system
INTERMEDIATE TERM REGULATION OF
BLOOD PRESSURE
1. Renin – Angiotensin system
INTERMEDIATE TERM REGULATION OF
BLOOD PRESSURE
INTERMEDIATE TERM REGULATION OF
BLOOD PRESSURE
1. Renin – Angiotensin system
INTERMEDIATE TERM REGULATION OF
BLOOD PRESSURE
2. Capillary shift mechanism
Movement of fluid from interstitial spaces into capillaries in
response to ↓ BP to maintain blood volume.
Conversely, when capillary pressure ↑ too high, fluid is lost
out of circulation into the tissues, reducing blood volume as
well as all pressures throughout circulation
INTERMEDIATE TERM REGULATION OF
BLOOD PRESSURE
2. Capillary shift mechanism
INTERMEDIATE TERM REGULATION OF
BLOOD PRESSURE
3 Stretch Relaxation of Vessels
Blood vessel smooth muscle respond to changes in blood
volume.
When pressure in blood vessels is “too high”, vessels
stretched and stretching more and more for minutes or hours;
resulting in decrease blood pressure in vessels toward normal.
The continuing stretch response of the vessels can serve as an
intermediate-term pressure “buffer.”
LONG TERM REGULATION OF BLOOD
PRESSURE (acting within days to months)
1. Renal Body fluid control mechanism
2. Aldosterone Mechanism
LONG TERM REGULATION OF BLOOD
PRESSURE
1. Renal Body fluid control mechanism
LONG TERM REGULATION OF BLOOD
PRESSURE
1. Renal Body fluid control mechanism
LONG TERM REGULATION OF BLOOD
PRESSURE
1. Renal Body fluid control mechanism
LONG TERM REGULATION OF BLOOD
PRESSURE
2. Aldosterone Mechanism
LONG TERM REGULATION OF BLOOD
PRESSURE
2. Aldosterone Mechanism
11- Arterial Blood Pressure Regulation.ppt

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11- Arterial Blood Pressure Regulation.ppt

  • 1. REGULATION OF BLOOD PRESSURE Prof. Sultan Ayoub Meo MBBS, Ph.D (Pak), M Med Ed (Dundee), FRCP (London), FRCP (Dublin), FRCP (Glasgow), FRCP (Edinburgh) Professor and Consultant, Department of Physiology, College of Medicine, King Saud University, Riyadh, KSA
  • 2.  Factors regulating arterial blood pressure  Explain how they influence arterial blood pressure.  Physiological importance of regulating arterial blood pressure  Discuss short term, intermediate and long-term regulation of blood pressure; nervous, hormonal and renal regulation of arterial blood pressure. LECTURE OBJECTIVES
  • 5. SHORT TERM REGULATION OF BLOOD PRESSURE 1. Baroreceptors Reflex Mechanism 2. Chemoreceptors Mechanism 3. CNS Ischemic Response Mechanism 4. Atrial Stretch Volume Receptors Rapidly acting within seconds to minutes
  • 6. 1. THE BARORECEPTORS Changes in MAP are detected by baroreceptors (pressure receptors) in the carotid and aortic arteries. Carotid baroreceptors are located in the carotid sinus, both sides of the neck. Aortic baroreceptors are located in the aortic arch. These receptors provide information to the cardiovascular centres in the medulla oblongata about the degree of stretch with pressure changes.
  • 7. Guyton and Hall, pp 174 1. THE BARORECEPTORS
  • 8.  At normal arterial pressure the baroreceptors are active.  Increased blood pressure increases their rate of activity, while decreased pressure decreases the rate of firing (activity).  They play an important role in maintaining relatively constant blood flow to vital organs such as brain during rapid changes in pressure such as standing up after lying down. That is why they are called “pressure buffers”. 1. THE BARORECEPTORS
  • 10. ↑ MAP Baroreceptors ↑ Parasympathetic (vagal) activity ↓ Sympathetic activity ↓ HR ↓ SV ↓ TPR ↓ MAP 1. THE BARORECEPTORS
  • 11. ↓ MAP Baroreceptors ↓ Parasympathetic (vagal) activity ↑ Sympathetic activity ↑ HR ↑ SV ↑ TPR  MAP 1. THE BARORECEPTORS
  • 13.  Baroreceptors are important in maintaining MAP constant during changes in body posture.  When change of posture from supine to erect, drop in the MAP in the head and upper part of the body.  The barorecptor reflex is activated → strong sympathetic impulses → vasoconstriction. This minimizes the drop in MAP. 1. THE BARORECEPTORS
  • 15. 2. THE CHEMORECEPTOR REFLEX  Chemoreceptors have high blood flow (1200 ml/min/g tissue). This makes it easy for these cells to detect changes in O2, CO2, and H+.  Reduced blood flow (due to reduced MAP) stimulates the chemoreceptors through oxygen lack, increased hydrogen ions or carbon dioxide.  Chemoreceptors are stimulated when the MAP is lower than 60 mmHg.  Response is excitatory, NOT inhibitory; mainly through activation of sympathetic nervous system.  They reduce blood flow to unessential areas and protect vital tissues like brain and heart.
  • 16. 3. CNS ISCHEMIC RESPONSE  CNS ischemic response operates rapidly to prevent further decrease in MAP whenever blood flow to the brain decreases.  It is one of the most powerful activators of the sympathetic vasoconstrictor system.  When MAP < 20 mmHg → cerebral ischemia of vasomotor center → strong excitation of vasomotor center (due to accumulation of CO2, lactic acid,) → strong vasoconstriction of blood vessels including the kidney arterioles.
  • 17. 4. ATRIAL STRETCH VOLUME RECEPTORS Receptors in large veins close to heart, walls of the atria (response of blood volume). An increased blood volume  stretch of atria  activate atrial volume receptors  sensory afferent nerves to medulla inhibiting the cardiovascular centre  This results into decreased blood volume through: (a)   sympathetic drive to kidney: -  dilate afferent arterioles   glomerular capillary hydrostatic pressure  GFR   blood volume (towards normal). -  renin secretion (Renin is an enzyme which activates angiotensinogen in blood). Inhibition of renin secretion  inhibit RAAS  inhibit aldosterone production   Blood volume (towards normal) (b)   ADH secretion   blood volume (towards normal). (c)   Atrial Natriuretic Peptide (ANP) causes loss of blood volume.
  • 18. INTERMEDIATE TERM REGULATION OF BLOOD PRESSURE 1. Renin – Angiotensin system 2. Capillary shift mechanism 3. Stretch relaxation of vessels Respond from 30 min to several hrs
  • 19. 1. Renin – Angiotensin system INTERMEDIATE TERM REGULATION OF BLOOD PRESSURE
  • 20. 1. Renin – Angiotensin system INTERMEDIATE TERM REGULATION OF BLOOD PRESSURE
  • 21. INTERMEDIATE TERM REGULATION OF BLOOD PRESSURE 1. Renin – Angiotensin system
  • 22. INTERMEDIATE TERM REGULATION OF BLOOD PRESSURE 2. Capillary shift mechanism Movement of fluid from interstitial spaces into capillaries in response to ↓ BP to maintain blood volume. Conversely, when capillary pressure ↑ too high, fluid is lost out of circulation into the tissues, reducing blood volume as well as all pressures throughout circulation
  • 23. INTERMEDIATE TERM REGULATION OF BLOOD PRESSURE 2. Capillary shift mechanism
  • 24. INTERMEDIATE TERM REGULATION OF BLOOD PRESSURE 3 Stretch Relaxation of Vessels Blood vessel smooth muscle respond to changes in blood volume. When pressure in blood vessels is “too high”, vessels stretched and stretching more and more for minutes or hours; resulting in decrease blood pressure in vessels toward normal. The continuing stretch response of the vessels can serve as an intermediate-term pressure “buffer.”
  • 25. LONG TERM REGULATION OF BLOOD PRESSURE (acting within days to months) 1. Renal Body fluid control mechanism 2. Aldosterone Mechanism
  • 26. LONG TERM REGULATION OF BLOOD PRESSURE 1. Renal Body fluid control mechanism
  • 27. LONG TERM REGULATION OF BLOOD PRESSURE 1. Renal Body fluid control mechanism
  • 28. LONG TERM REGULATION OF BLOOD PRESSURE 1. Renal Body fluid control mechanism
  • 29. LONG TERM REGULATION OF BLOOD PRESSURE 2. Aldosterone Mechanism
  • 30. LONG TERM REGULATION OF BLOOD PRESSURE 2. Aldosterone Mechanism