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15. BLOOD PRESSURE REGULATION- HYPERTENSION

Cardiovascular: Blood Pressure Regulation- Hypertension Medical Editor: Donya Moslemzadeh

OUTLINE BARORECEPTOR REFLEX

Response to High Blood Pressure:
I) INTRODUCTION
II) BARORECEPTORS
When Pressure is HIGH→ ↑stretch on
III) RENAL REGULATION
vessel wall→ ↑ stretch of sensory nerve
IV) ATRIAL NATRIURETIC PEPTIDE (ANP)
V) REFRENCES endings of Aortic Sinus and Carotid
Sinus→ ↑ activation of mechanically
gated Na+ channels→ ↑ Na+ enters
nerve endings→ ↑ action potentials are
carried down Glossopharyngeal and
I) INTRODUCTION Vagus sensory fibers→ Medulla→ Nucleus Tractus
Solitarius (NTS)
Hypertension
Definition: High Blood Pressure Nucleus Tractus Solitarius (NTS)
o Systolic Blood Pressure, SBP>140mmHg o This is a relay center
o Diastolic Blood Pressure, DBS >90mmHg o Signals from the Vagus and glossopharyngeal nerve
Normal Blood Pressure [UpToDate]  NTS→ (+) Cardiac Inhibitory Center in medulla
o Systolic Blood Pressure: < 120  NTS→ (-) Cardio acceleratory Center in Medulla
o Diastolic Blood Pressure: < 80  NTS→ (-) Vasomotor Center in Medulla
Physiological response to Hypertension
o Baroreceptor reflex
o Inhibition of Renin-Angiotensin- Aldosterone System

Formulas & Relations: Vasomotor center has 2 important areas:

𝐵𝐵𝐵𝐵 = 𝐶𝐶𝐶𝐶 × 𝑇𝑇𝑇𝑇𝑇𝑇
𝐶𝐶𝐶𝐶 = 𝐻𝐻𝐻𝐻 × 𝑆𝑆𝑆𝑆 1) C1 is for constriction of the
𝑅𝑅 = 8𝜂𝜂𝜂𝜂 ⁄𝜋𝜋𝑟𝑟 4 vessels, activated when the
blood pressure is low and
inhibited when the blood
↑Heart rate→↑CO
pressure is high
↓Heart Rate→↓CO
↑EDV→↑SV→↑CO
2) A1 is for vasodilation of the
↓EDV→↓SV→↓CO
vessels , activated when
↑ESV→↓SV→↓CO
the blood pressure is high and inhibited when
↓ESV→↑SV→↑CO
the blood pressure is low
↑Preload→↑SV→↑CO
↓Preload→↓SV→↓CO
↑Contractility→↑ SV→↑ CO
↓Contractility→↓SV→↓CO
↑Afterload→↓SV→↓CO
↓Afterload→↑SV→↑CO
↓Vessel Radius→↑Peripheral Vascular Resistance
↑Vessel radius→↓Peripheral Vascular Resistance

II) BARORECEPTORS
Definition: Stretch-sensitive nerve endings
Location: AfraTafreeh.com
o Aortic Arch
 Around Aortic Arch there is Aortic Sinus that is
sensitive to pressure changes.
 Aortic Sinus are innervated by sensory fibers of
Cranial Nerve X (Vagus nerve)

o Bifurcation of Common Carotid Artery

 Around Bifurcation there is Carotid sinus that are
sensitive to Pressure changes Figure 1. Baroreceptor reflex in High BP.
 Carotid Sinus are innervated by sensory fibers of
Cranial Nerve IX (Glossopharyngeal Nerve)

Blood Pressure Regulation- Hypertension CARDIOVASCULAR PHYSIOLOGY : Note #15. 1 of 4

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(1) Cardio- Inhibitory Center (3) Vasomotor Center
= Dorsal Nucleus Vagus Part of the Sympathetic Nervous system
Part of Parasympathetic Nervous System Inhibited due to Low Blood Pressure signal coming
Stimulated due to High Blood Pressure signal coming through Sensory afferent fibers of CN X and CN IX to the
through Sensory afferent fibers of CN X and CN IX to the NTS
NTS o Inhibits Sympathetic Nervous system→
Activates Parasympathetic Nervous system→ ↓Norepinephrine release→ ↓ stimulation of alpha-1
↑Acetylcholine release→ stimulates M2-Receptors on Receptors on smooth muscle cells (Tunica Media) in
nodal cells→ ↓HR→ ↓Cardiac Output→ ↓Blood pressure arterioles→ Vasodilation of arterioles→ ↑Vessel
o Right Vagus → SA node diameter→ ↓Resistance→↓Blood pressure (Diastolic
o Left Vagus → AV node Blood Pressure)
No innervation to myocardium from the Vagus Nerve
Changing Total Peripheral Resistance= Changing
M2 Receptor → Gi → Inhibits AC → ↓cAMP → ↓PKA → Diastolic Blood Pressure
inhibits Ca2+ channels→ ↓ Ca2+→ Hyperpolarization
M2 Receptor → βi and γi → Activates K+ Channels → K+
Adrenal Medulla
leaking out of the cell → Hyperpolarization Inhibited Sympathetic Nervous system → Adrenal
Medulla → Chromaffin Cells →↓production of
Epinephrine (80%) and Norepinephrine (20%) →
↓↓ Stimulation Beta-1 and Alpha-1 receptors→ ↓HR,
↓Contractility, Vasodilation →↓Blood pressure

III) RENAL REGULATION

The kidneys act both directly and indirectly to regulate
Blood pressure: [Marieb & Hoehn, 2012]
Direct Renal Mechanism
o The direct renal mechanism alters blood volume
independently of hormones. When either blood
volume or blood pressure rises, the rate at which fluid
Figure 2. M2 Receptor mechanism. filters from the bloodstream into the kidney tubules
speeds up. In such situations, the kidneys cannot
reabsorb the filtrate rapidly enough, and more of it
leaves the body in urine. As a result, blood volume
Good to Know: and blood pressure fall. [Marieb & Hoehn, 2012]
o ↑↑ Systemic BP (SBP>140mmhg) → ↑Hydrostatic
Chronotropy: Any influence on Heart Rate [AMBOSS]] Pressure in Glomerulus→ ↑GFR→ ↑Urine output→
o Positive Chronotropic action ↓Blood Volume→ ↓BP
 SNS→ NE, Epi → ↑HR Indirect Renal Mechanism
o Negative Chronotropic action
o Renin-Angiotensin-Aldosterone System
 PSNS → Ach → ↓HR
Inotropy: Any influence on Myocardial contraction
[AMBOSS] RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
o Positive Inotropic action
 SNS → NE, Epi → ↑Contractility (1) Production of Angiotensin-II
o Negative Inotropic action →↓ Contractility
Components:
o Renin
 Enzyme produced by the kidneys
o Angiotensinogen
 Protein produced by the liver
(2) Cardio- Acceleratory Center  circulates in the blood
Part of Sympathetic Nervous System o Angiotensin-I
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Inhibited due to High Blood Pressure signal coming  Precursor molecule
through Sensory afferent fibers of CN X and CN IX to the o Angiotensin Converting Enzyme (ACE)
NTS  Mostly Produced by Vascular endothelial cells of
the lungs
o Inhibits Sympathetic Nervous system→ o Angiotensin-II
↓Norepinephrine release→ ↓Stimulation of Beta 1
(2) Angiotensin-II Action Pathways
Receptors on nodal cells (SA & AV nodes) →↓HR→
↓Cardiac Output→ ↓Blood pressure (i) Vasoconstriction
o Inhibits Sympathetic Nervous system→
↓Norepinephrine release→ inhibits Beta 1 Receptors o Angiotensin-II receptors on the Tunica Media of the
on contractile cells→ ↓Contractility→ ↓Stroke Arterioles
volume→ ↓Cardiac output→ ↓Blood pressure o Angiotensin-II stimulates Vasoconstriction of Systemic
Arterioles→↓Vessel Diameter→ ↑Resistance→ ↑BP

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(ii) ALDOSTERONE IV) ATRIAL NATRIURETIC PEPTIDE (ANP)
o Steroid Hormone Produced by Zona Glomerulosa of Definition: A peptide hormone released from atrial
the adrenal medulla myocytes in response to increased stretch on the atrium
o Angiotensin-II Stimulates Aldosterone Production
[AMBOSS]
from Adrenal Cortex→ Aldosterone ↑Na+ and H20 Natriuretic= Producing Salty Urine
reabsorption in Distal Convoluted Tubules of kidney→
↑ Blood Volume→ ↑BP Response to High Blood Pressure
↑↑ BP→ Stretches atrial chambers→ stimulates release
o Mechanism of Action of Aldosterone of Atrial Natriuretic Peptide (ANP)→ ↓Renin Angiotensin
 Acts on Distal Convoluted Tubules Aldosterone ADH Axis
 Aldosterone binds to the intracellular receptor→
activate specific Genes → ↑production of 3 ANP→ ↓Angiotensin II pathways
Proteins
(i) Vasodilation
Na+ Channels
o ANP blocks Angiotensin II→ ↑Vasodilation of
o More Na+ flows to the cells
Systemic Arterioles→↑Diameter→↓Resistance→↓BP
K+ Channels
o More K+ flows out of the cells to the Distal (ii) Decrease blood volume
Convoluted Tubules
o ANP→↓Angiotensin II→↓Aldosterone Production
Na+ / K+ / ATPase Pump (on Basolateral Membrane)
from Adrenal Cortex→↓Na+ and H20 reabsorption in
o 3 Na+ reabsorbed to the circulation in
Distal Convoluted Tubules→↓Blood Volume→↓BP
exchange of 2 K+
 H2O follows Na+ back to the circulation
o ANP→↓Angiotensin II→↓ADH release from Posterior
(iii) ADH Pituitary→↓water reabsorption in Collecting
duct→↓Blood Volume→↓BP
o ADH =Anti-Diuretic Hormone= Vasopressin
o Supraoptic nucleus (specials cells in the
o ANP→↓Angiotensin II→↓Hypothalamic thirst center
Hypothalamus) → Posterior Pituitary glands→
activity→↓consumption of water→↓absorption across
Release of ADH
GIT→↓Blood Volume→↓BP
o Angiotensin-II Stimulates Posterior Pituitary→ ↑ADH
release→ ↑water reabsorption in Collecting duct of
o ANP→↓Angiotensin II→↓Na+ and H20 reabsorption in
kidneys→ ↑Blood Volume→ ↑BP
Proximal Convoluted Tubules→↓Blood Volume→↓BP
o Mechanism of Action of ADH
 Acts on 2 locations in the nephron ↓Na+ and H20 reabsorption→ ↑ Urine output = Polyuria
• Collecting duct
• Distal Convoluted Tubules
 ADH binds to V2-Receptore (Gs-Protein) → AC →
cAMP → PKA → Phosphorylation vesicles
containing AQ-II → ↑ express of AQ-II on the
membrane → ↑ reabsorption of H2O

(iv) Thirst Center

o Angiotensin-II→↑ Hypothalamic thirst center
activity→↑consumption of water→↑absorption across
GIT→ ↑ Blood Volume→ ↑ BP

(v) Kidney
o Angiotensin-II→↑ Na+, Cl- and H20 reabsorption in
Proximal Convoluted Tubules of kidney→ ↑ Blood
Volume→ ↑ BP
(3) Response to High Blood Pressure
↑↑Systemic BP (SBP>140mmhg)→ ↓ Renin Angiotensin
Aldosterone ADH Axis
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↑↑ BP→ ↓ Juxtaglomerular cell activity in the Afferent
arteriole of glomerulus→ ↓ Renin release
↑↑ BP→ ↓sympathetic nervous system activity→↓B1
activity on Juxtaglomerular cells in the Afferent arteriole
of glomerulus→ ↓Renin release Figure 3. Sites of action of ADH, Aldosterone, Angiotensin-II
↑↑ BP→ ↑GFR→ ↑Na+ and Cl- levels in tubules Macula and ANP on a nephron.
Densa cells in distal convoluted Tubules→ ↓release of
PGE2→ ↓Juxtaglomerular cell activity in the Afferent
arteriole of glomerulus→ ↓release of Renin

Blood Pressure Regulation- Hypertension CARDIOVASCULAR PHYSIOLOGY : Note #15. 3 of 4

 Figure 4. Physiologic Responses to High Blood Pressure.

V) REFRENCES
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● Marieb, E. N., & Hoehn, K. N. (2012). Human Anatomy &
Physiology (9th Edition) (Marieb, Human Anatomy &
Physiology) (9th ed.). Pearson.
● Hall, J. E., & Hall, M. E. (2020). Guyton and Hall Textbook of
Medical Physiology (Guyton Physiology) (14th ed.). Elsevier.
● AMBOSS: medical knowledge platform for doctors and students.
(n.d.). Amboss. Retrieved August 9, 2021, from
https://www.amboss.com/us/
● Boron, W. F., & Boulpaep, E. L. (2016). Medical Physiology (3rd
ed.). Elsevier.
● Mohrman, D. E., & Heller, L. J. (2018). Cardiovascular
Physiology (9th ed.). McGraw-Hill Education / Medical.
● UpToDate: Evidence-based Clinical Decision Support. (n.d.).
Uptodate. Retrieved August 16, 2021, from
http://www.uptodate.com/index

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