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Mean Arterial
Blood Pressure
Regulation
PHYSIOLOGICAL MECHANISMS AND
PROCESSES
KEY TOPICS:
▪ Purpose of blood pressure regulation
mechanisms
▪ Blood pressure measurement (systolic,
diastolic, MAP)
▪ Short-term control mechanisms:
baroreceptor reflex, chemoreceptor reflex,
hormones
▪ Cardiovascular Regulatory Center
▪ Long-term control mechanisms: RAAS –
Why Is There a Need for Blood Pressure Regulation?
HOMEOSTASIS:
property of a biological system whereby it regulates its inter
vironment in response to changing external stimuli in order
in a stable, relatively constant condition of properties that su
long-term survival.”
Why Is There a Need for Blood Pressure Control?
Examples of Homeostatic Control:
• Body temperature (~98.6° F)
• Blood pH (~7.35-7.45)
• Fasting blood sugar (~70-99 mg/dL)
• Blood Pressure (~120/80 mm Hg)
Blood Pressure Measurement
Systolic Pressure:
Peak pressure, occurs as left
ventricle fully contracts and
expands the aorta.
Diastolic Pressure:
Lowest pressure, reached when
aortic valve closes at end of left
ventricle contraction and vessels
rebound (contract) as blood
“Blood pressure fluctuates in a cardiac
Mean Arterial Blood Pressure (MAP)
MAP = Diastolic BP + 1/3(Pulse Pressure)
Pulse Pressure = Systolic – Diastolic
120/80 mm Hg MAP =
80 + 1/3(40) = 93 mm Hg
BP Regulation Mechanisms
a. Baroreceptor Reflex
I. Short Term Mechanisms (fraction of sec
b. Chemoreceptor Reflex
c. Hormone action (ADH, ANP, Epinephrine, Nore
BP Regulation Mechanisms
Renin – Angiotensin – Aldosterone System
II. Long Term Mechanism (minutes to days
Cardiovascular Regulatory Center
• Located in medulla oblongata
• Part of the Nucleus Tractus Solitari (NTS)
• Autonomic control of heart and blood ves
and vasomotor centers)
• Receives stimuli from specialized sensory
• In response, modulates sympathetic and
signals (excites or inhibits) to heart and
Cardiovascular Regulatory Center Actions
Baroreceptor Reflex
acting, negative feedback loop that seeks to maintain cons
ood pressure especially during sudden postural changes. Ac
faster than a single cardiac cycle (< 1 second).
Baroreceptor Reflex
Baroreceptors:
• Kinesthetic sensory neurons (mechanorece
• Synapse with Nucleus Tractus Solitari in CV
• Sense pressure at carotid sinuses and aort
• Detect changes in blood vessel diameter:
• Expansion  Increased BP;
• Contraction Decreased BP
• Active during homeostasis as well
Baroreceptor Reflex
CAROTID SINUS
BARORECEPTORS
Detect stretch at the
carotid sinuses. Innervated
by the Glossopharyngeal
Nerve (CN IX) via the sinus
nerve of Hering and
synapse with the CVRC.
Baroreceptor Reflex
AORTIC ARCH
BARORECEPTORS
Detect stretch in the
ascending
aorta. Innervated by the
aortic nerve, branches with
the Vagus Nerve
(CN X) and synapses with
the
Baroreceptor Reflex Effect on BP
INCREASING (^) BLOOD PRESSURE:
^diameter  ^ firing rate  CVRC
excites PARASYMPATHETICS &
inhibits sympathetics to the
sinoatrial (SA) node resulting in v
HR, v force of contraction &
vasodilationDECREASING (v) BLOOD
PRESSURE:
v diameter  v firing rate  CVRC
excites SYMPATHETICS & inhibits
parasympathetics resulting in ^ HR,
^ force of contraction &
Chemoreceptor Reflex
cells in the aortic and carotid bodies (“peripheral” chemorec
edulla (“central” chemoreceptors) detect changes in O2, CO
s in the blood and CSF*, send action potentials to the cardio
ory center which then modulates parasympathetic and symp
on to the heart and blood vessels to return blood pressure c
homeostatic levels.
*central chemoreceptors in medulla sense CO2 and pH of CSF
Carotid and Aortic Bodies
“Glomus Cells”
Chemoreceptor Reflex Effect on BP
CN IX afferents
CN X afferents
CN X (efferents)
Sympathetic chain
• Glomus cells ^ release
of
neurotransmitters
• Excite CN IX and X
afferents to
cardiovascular
regulatory center
• Inhibits
parasympathetics
Scenario:
v O2, ^ CO2, v
pH
Chemoreceptor Reflex Effect on BP
Scenario:
v O2, ^ CO2, v
pHCauses:
• Increase in HR
• Increase in force of contra
• Vasoconstriction
Hormonal Effects on BP – Atrial Natriuretic Peptide
• Secreted by atrial muscle cells in
to high blood volume/pressure
• Acts on kidneys to increase Na+
• Causes water and adipose loss vi
• Inhibits renin and aldosterone pr
• Decreases blood volume, vasodila
and lowers blood pressure
Hormonal Effects on BP – Epinephrine, Norepinephrine
• Also called adrenaline, noradren
• Produced in the adrenal medulla
response to stressors and symp
simulation (“fight or flight”)
• Increases HR, force of contractio
therefore blood pressure
• Vasoconstricts small vessels; va
vessels in skeletal muscle and li
Hormonal Effects on BP – Vasopressin
• Also known as Anti Diuretic Horm
• Produced in the posterior pituita
• Released when blood pressure d
• Causes reabsorption of Na+ in r
• Results in water retention
• Increases blood volume and pre
• Vasoconstricts blood vessels
Long Term Blood Pressure Regulation:
Renin-Angiotensin-Aldosterone System
• Engages when the cause of blood pressure drop is long
• Hemorrhage, dehydration, Na+ deficiency
• Involves kidneys and liver working to increase product
Antgiotensin II, a powerful vasoconstrictor
• Control mechanism is via measured release of Renin in
by the juxtaglomerular cells of the kidneys which initia
Angiotensin II.
Long Term Blood Pressure Regulation:
Renin-Angiotensin-Aldosterone System
What Causes JGCs to
Release Renin?
1. Decreased perfusion to
kidneys
2. Macula densa cells detect
drop in Na+ and secrete
prostaglandin, triggers JGCs
3. Sympathetic stimulation to
JGCs
Long Term Blood Pressure Regulation:
Renin-Angiotensin-Aldosterone System
Angiotensin II
NET EFFECT:
1. Vasoconstriction of
arterioles
2. Increase in
Aldosterone,
3. Increase Na+, H2O
reabsorp.
4. Increase ADH
release
Question and Answer Period

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Maintaining homeostatic mean arterial blood pressure

  • 2. KEY TOPICS: ▪ Purpose of blood pressure regulation mechanisms ▪ Blood pressure measurement (systolic, diastolic, MAP) ▪ Short-term control mechanisms: baroreceptor reflex, chemoreceptor reflex, hormones ▪ Cardiovascular Regulatory Center ▪ Long-term control mechanisms: RAAS –
  • 3. Why Is There a Need for Blood Pressure Regulation? HOMEOSTASIS: property of a biological system whereby it regulates its inter vironment in response to changing external stimuli in order in a stable, relatively constant condition of properties that su long-term survival.”
  • 4. Why Is There a Need for Blood Pressure Control? Examples of Homeostatic Control: • Body temperature (~98.6° F) • Blood pH (~7.35-7.45) • Fasting blood sugar (~70-99 mg/dL) • Blood Pressure (~120/80 mm Hg)
  • 5. Blood Pressure Measurement Systolic Pressure: Peak pressure, occurs as left ventricle fully contracts and expands the aorta. Diastolic Pressure: Lowest pressure, reached when aortic valve closes at end of left ventricle contraction and vessels rebound (contract) as blood “Blood pressure fluctuates in a cardiac
  • 6. Mean Arterial Blood Pressure (MAP) MAP = Diastolic BP + 1/3(Pulse Pressure) Pulse Pressure = Systolic – Diastolic 120/80 mm Hg MAP = 80 + 1/3(40) = 93 mm Hg
  • 7. BP Regulation Mechanisms a. Baroreceptor Reflex I. Short Term Mechanisms (fraction of sec b. Chemoreceptor Reflex c. Hormone action (ADH, ANP, Epinephrine, Nore
  • 8. BP Regulation Mechanisms Renin – Angiotensin – Aldosterone System II. Long Term Mechanism (minutes to days
  • 9. Cardiovascular Regulatory Center • Located in medulla oblongata • Part of the Nucleus Tractus Solitari (NTS) • Autonomic control of heart and blood ves and vasomotor centers) • Receives stimuli from specialized sensory • In response, modulates sympathetic and signals (excites or inhibits) to heart and
  • 11. Baroreceptor Reflex acting, negative feedback loop that seeks to maintain cons ood pressure especially during sudden postural changes. Ac faster than a single cardiac cycle (< 1 second).
  • 12. Baroreceptor Reflex Baroreceptors: • Kinesthetic sensory neurons (mechanorece • Synapse with Nucleus Tractus Solitari in CV • Sense pressure at carotid sinuses and aort • Detect changes in blood vessel diameter: • Expansion  Increased BP; • Contraction Decreased BP • Active during homeostasis as well
  • 13. Baroreceptor Reflex CAROTID SINUS BARORECEPTORS Detect stretch at the carotid sinuses. Innervated by the Glossopharyngeal Nerve (CN IX) via the sinus nerve of Hering and synapse with the CVRC.
  • 14. Baroreceptor Reflex AORTIC ARCH BARORECEPTORS Detect stretch in the ascending aorta. Innervated by the aortic nerve, branches with the Vagus Nerve (CN X) and synapses with the
  • 15. Baroreceptor Reflex Effect on BP INCREASING (^) BLOOD PRESSURE: ^diameter  ^ firing rate  CVRC excites PARASYMPATHETICS & inhibits sympathetics to the sinoatrial (SA) node resulting in v HR, v force of contraction & vasodilationDECREASING (v) BLOOD PRESSURE: v diameter  v firing rate  CVRC excites SYMPATHETICS & inhibits parasympathetics resulting in ^ HR, ^ force of contraction &
  • 16. Chemoreceptor Reflex cells in the aortic and carotid bodies (“peripheral” chemorec edulla (“central” chemoreceptors) detect changes in O2, CO s in the blood and CSF*, send action potentials to the cardio ory center which then modulates parasympathetic and symp on to the heart and blood vessels to return blood pressure c homeostatic levels. *central chemoreceptors in medulla sense CO2 and pH of CSF
  • 17. Carotid and Aortic Bodies “Glomus Cells”
  • 18. Chemoreceptor Reflex Effect on BP CN IX afferents CN X afferents CN X (efferents) Sympathetic chain • Glomus cells ^ release of neurotransmitters • Excite CN IX and X afferents to cardiovascular regulatory center • Inhibits parasympathetics Scenario: v O2, ^ CO2, v pH
  • 19. Chemoreceptor Reflex Effect on BP Scenario: v O2, ^ CO2, v pHCauses: • Increase in HR • Increase in force of contra • Vasoconstriction
  • 20. Hormonal Effects on BP – Atrial Natriuretic Peptide • Secreted by atrial muscle cells in to high blood volume/pressure • Acts on kidneys to increase Na+ • Causes water and adipose loss vi • Inhibits renin and aldosterone pr • Decreases blood volume, vasodila and lowers blood pressure
  • 21. Hormonal Effects on BP – Epinephrine, Norepinephrine • Also called adrenaline, noradren • Produced in the adrenal medulla response to stressors and symp simulation (“fight or flight”) • Increases HR, force of contractio therefore blood pressure • Vasoconstricts small vessels; va vessels in skeletal muscle and li
  • 22. Hormonal Effects on BP – Vasopressin • Also known as Anti Diuretic Horm • Produced in the posterior pituita • Released when blood pressure d • Causes reabsorption of Na+ in r • Results in water retention • Increases blood volume and pre • Vasoconstricts blood vessels
  • 23. Long Term Blood Pressure Regulation: Renin-Angiotensin-Aldosterone System • Engages when the cause of blood pressure drop is long • Hemorrhage, dehydration, Na+ deficiency • Involves kidneys and liver working to increase product Antgiotensin II, a powerful vasoconstrictor • Control mechanism is via measured release of Renin in by the juxtaglomerular cells of the kidneys which initia Angiotensin II.
  • 24. Long Term Blood Pressure Regulation: Renin-Angiotensin-Aldosterone System What Causes JGCs to Release Renin? 1. Decreased perfusion to kidneys 2. Macula densa cells detect drop in Na+ and secrete prostaglandin, triggers JGCs 3. Sympathetic stimulation to JGCs
  • 25. Long Term Blood Pressure Regulation: Renin-Angiotensin-Aldosterone System Angiotensin II NET EFFECT: 1. Vasoconstriction of arterioles 2. Increase in Aldosterone, 3. Increase Na+, H2O reabsorp. 4. Increase ADH release