+

Blood Pressure
Regulation
Amira Abd Jamil

[email protected]
+ Blood pressure (BP): Definition

◼ Refers to the pressure in the arteries/aorta = Pressure exerted by

the blood in the inner wall of the blood vessels
◼ Achieved during ventricular contraction (systolic pressure), and
relaxation phase of cardiac cycle (diastolic pressure).

◼ In healthy resting adult, systolic pressure is approximately 120 -140

mmHg (highest pressure in the artery/aorta) and diastolic pressure is
approximately 70 - 90 mmHg (lowest pressure in artery/aorta)

◼ Average blood pressure in an individual: MEAN ARTERIAL BP (MAP)

◼ MAP = 1/3 pulse pressure + diastolic BP, where pulse pressure = Systolic
BP – diastolic BP

◼ MAP = 1/3 (systolic BP – diastolic BP) + diastolic BP

+
Blood pressure depends on 2 factors:

BP = Cardiac output (CO) x Total peripheral resistance (TPR)

= Stroke volume (SV) x Heart rate (HR) x TPR

Understanding how the major systemic hemodynamic variables are

regulated in the above equation is a prerequisite to understand the
overall regulation of blood pressure.
+ TOTAL PERIPHERAL RESISTANCE
◼ The sum of all vascular
resistance within the
systemic circulation is
called the total
peripheral resistance
(TPR)

◼ Arterioles contain a high

proportion of vascular
smooth muscle and
hence the arteriolar
diametre is a major
component of TPR.

→ Contraction of arteriolar
vascular smooth muscle = Total resistance opposing the
decreases vascular blood flow in the systemic
diametre and increases circulation
vascular resistance
+ Venoconstriction and
vasoconstriction
IN ARTERIES VS VEINS

▪At rest, 64% of blood are

pooled in the venous system
(blue)

▪ therefore, the constriction

of of the veins will push the
blood to go back into the
right atrium
→ increase venous return
+
Regulation of blood pressure
◼ Why is it important to maintain BP?
→ To maintain adequate normal blood flow and thus perfusion to the
tissues

◼ Mean BP is regulated within normal limits by 2 main

mechanism:
1. Short term/ fast neural reflex mechanism
◼ Baroreceptor reflex mechanism
◼ Chemoreceptor reflex mechanism

2. Long term pressure regulation

◼ Renin angiotensin system and the kidney
→ Regulates blood volume/ECF volume
+
Regulation of blood pressure:

SHORT TERM/FAST
NEURAL REFLEX
Baroreceptor reflex mechanism
+ CARDIOVASCULAR CENTRE (CVC)
• Integrating Cardiovascular Centre (CVC):
located in the In the medulla oblongata,
integrate impulse from other areas in the
brain.

▪ The organisation of CVC is unclear, but

important areas in the CVC are
▪ NTS (nucleus of tractus solitaries) –
receives impulse from the vagus and
Glossopharyngeal nerves. The impulse
from NTS helps to control the activity of
cardiac acceleratory centre (CAC) and
cardio inhibitory centre (CIC).

▪ CAC/vasomotor centre – transmits

excitatory impulse to the heart and blood
vessel via the sympathetic nerves

▪ CIC – transmit inhibitory impulse to the

heart via the parasympathetic nerve
+ 1. Baroreceptor reflex
▪ Baroreceptors- High pressure sensors , respond to stretch
caused by blood pressure – induce rapid reflex via the
autonomic nervous system

▪ Located in :
i) aortic arch
ii) carotid sinus (birufication of common carotid artery)

▪ Afferent innervation - sensory impulses from the aortic arch

baroreceptors travel in the vagus nerve (cranial nerve X )
while those from carotid sinus travel via the
glossopharyngeal nerve (cranial nerve IX )

▪ Impulse are sent to and terminates at NTS in the medulla

oblongata
+
 Baroreceptor reflex: following increased BP
+ 1. Increase in blood pressure → causes distension of aorta and carotid arteries,
baroreceptors are stimulated

Information is relayed through the vagus and glossopharengeal nerve. Impulse are
sent to and terminates at NTS in the medulla oblongata. NTS stimulates activity of CIC
and increase parasympathetic activity to the heart.

• Cardioinhibitory centres in the medulla Vasomotor centre and CAC in medulla oblongata are
oblongata are stimulated – and inhibited – vasomotor and CAC send fibres to the
increases parasympathetic activity to sympathetic nerves of the lateral horns cells of the
the heart spinal cord

• Parasympathetic activity innervates SA 1. Inhibitory impulse to the vasomotor sensor

node AV node. Parasympathetic activity decreases sympathetic vasoconstrictor tone to
release acetylcholine which acts on the blood vessel:
muscarinic receptors on the : • vasodilation → decreases TPR
1. SA node → cause a decrease in HR • venodilation → decreases VR
2. AV node →cause an increase in AV
nodal delay 2. Decreased sympathetic discharge to ventricular
muscle:
HENCE: decreased HR lowers BP by • Decreased contractility → decreases SV
lowering cardiac output
HENCE: decreased SV and TPR → lower BP
 Baroreceptor reflex: following decreased BP
+
2. Decrease in blood pressure → baroreceptors decrease rate of firing in the afferent neurons
of the vagus and glossopharengeal nerve. Impulse are sent to and terminates at NTS in the
medulla oblongata. NTS stimulates activity of CAC/ VMC and increase sympathetic
activity to the heart and blood vessels

Vasomotor centres and CAC in medulla

• Activity of cardioinhibitory centres in oblongata are stimulated – vasomotor centre
the medulla oblongata are decreased and CAC send fibres to the sympathetic nerves
while cardioaccelerator centre are of the lateral horns cells of the spinal cord
stimulated – increase sympathetic
activity to the heart. 1. Excitatory impulse to the vasomotor centre
• Sympathetic activity innervates SA increases sympathetic vasoconstrictor tone
node AV node. Sympathetic activity to blood vessel
release noradrenaline which acts on • Vasoconstriction → increases TPR
the β1-adrenpreceptors on the : • In the veins→ Venoconstrctition → increases
VR
1. SA node → increases HR
2. AV node → decreases AV nodal delay 2. Increased sympathetic discharge to ventricular
muscle
• Increased heart contractility hence an
HENCE: increased HR increases BP by increase in SV
increasing cardiac output HENCE: Increased VR, increased SV, increases
TPR → net effect of increased BP
+
+

RECALL: Autonomic
innvervation of the
heart!
+

Neural
regulation of the
heart
+ EFFECT: Parasympathetic input - HEART

ACTIONS MECHANISM
• Vagus nerve releases • Muscarinic receptors
ACH (M2)
• SA node and AV node – ßγ subunit (HR)
• HR and conduction
velocity
+ EFFECT: Sympathetic input - HEART

ACTIONS MECHANISM
• Nerve fibers release NA • ß1 adrenoreceptors
• SA, atria, and ventricles receptors – pacemaker
• ↑ HR and contractility activity
– R side SA node • ß1 adrenoreceptors
– L side contractility myocardium
contraction
+ EFFECT: Sympathetic input – Blood vessels

ACTIONS MECHANISM
• Activated - • Noradrenaline
Vasoconstriction blood – α>ß
vessel most abundant • Adrenaline
• Deactivated – – ß>α
Vasodilation
Vasoconstriction – α1
adrenoreceptors
Vasodilation – ß2
adrenoreceptors
+ Venoconstriction and
vasoconstriction

▪At rest, 64% of blood are

pooled in the venous system
(blue)

▪ therefore, the constriction

of of the veins will push the
blood to go back into the
right atrium
→ increase venous return
+
Regulation of blood pressure:

HORMONAL/ LONG
TERM REGULATION
1. The Renin Angiotensin Aldosterone System (RAAS)
2. Atrial Natriuretic Peptide
+ Long term regulation
▪ Mechanism for long term BP regulation: occurs though blood volume
regulation.

▪ Blood volume → major determinant of venous pressure, venous return,

hence EDV, SV and cardiac output.
▪ Increased blood volume → increase venous return → increase BP
▪ Decreased blood volume → decreases venous return → decreases BP

▪ Blood volume is determined by the amount of water and sodium ingested

and the amount of water loss and excreted by the kidney.

▪ The amount of blood volume → is affected by changes in total amount of

water and sodium which are regulated by the kidney.

▪ The primary mechanism by which the kidneys regulate blood volume

within normal ranges by controlling the excretion and water loss into the
urine by activating the renin-angiotensin-aldosterone system, antidiuretic
hormone and effect of atrial natriuretic peptide hormone.
+ Long term regulation
1. The Renin-angiotensin-aldosterone system (RAAS)

▪ Decreased in systemic blood pressure – decreased renal blood flow

stimulates secretion of hormone renin from the juxtaglomerular cells
within in each nephron in the kidney (refer diagram next slide).

▪ Renin is also released in response to sympathetic stimulation

Renin –

1. Splits plasma protein angiotensinogen (synthesized by the liver) to

angiotensin I.

2. Angiotensin I is converted to angiotensin II by an enzyme called the

angiotensin converting enzyme (ACE), secreted by the lung tissue
and vascular endothelium.
+ Kidney and the nephron
+ Juxtagromerular apparatus
+ EFFECT OF Angiotensin II
1. Stimulates the adrenal cortex to secrete aldosterone – causes conservation
of sodium and secretion of potassium in the distal tubes and collecting
ducts of the nephron → increases reabsorption of ions and water in the
kidney, hence cause water retention and increases blood volume.

2. Increases the secretion of anti-diuretic hormone (vasopressin) from the

posterior pituitary, increase permeability of the collecting tubules to water
→ increase water reabsoption and blood volume.

3. Stimulates thirst centre in the hypothalamus → increases fluid intake and

blood volume.

4. Potent vasoconstrictor of vascular smooth muscle in the blood vessel,

increases TPR

5. Enhances the release of norepinephrine from sympathetic nerves fibres

present in blood vessels.

→ The increase in ECF volume increases blood volume, and increases venous
return, hence SV and CO.
+
+ Long term regulation (cont)
3. Artrial natriuretic peptide (ANP)

▪ Released by the secretory granules in atria in response

to arterial stretch as blood pressure increases
▪ ANP promotes natiruresis and diuresis thus decrease
plasma volume and lowers blood pressure.

▪ → In kidney, it increases glomerular filtration rates and

inhibits tubular sodium reabsorption, leading to
increased urinary loss of water.

▪ ANP also decreases the release of ADH, renin and

aldosterone.
+ Speed and strength of response of
blood pressure regulation:

◼ The short term mechanism → is the first line

defense against abnormal BP. act very quickly
(e.g. the baroreceptors act within one
heartbeat)

◼ The control of blood volume by the kidneys acts

on a time scale of hours and even days
 Speed and strength of response of
+ blood pressure regulation
Summary
▪ BP is determined by cardiac output and total peripheral resistance

▪ Regulatory mechanisms depends on fast-acting reflexes which control

heart rate, stroke volume, and total peripheral resistance.

▪ Fast acting reflex mechanism

• baroreceptor reflex
• chemoreceptor reflex
• adrenal medullary hormones
▪ Long-term mechanisms are mainly concerned with regulation of body
fluids and blood volume
• renin-angiotensin system
• aldosterone secretion
• vasopressin antidiuretic effect
• ANP secretion
Summary
 Thank you for
your attention!