9

Color Index:
• Main text
• Important
Arterial Blood Pressure • Girls Slides
• Boys Slides
• Notes
& Its Regulation • Extra

Editing File
Objectives
Concept & definition of blood pressure.& Normal values of systolic & diastolic blood pressure.

Physiological variations in arterial blood pressure. & Pulse & Mean arterial pressures. Factors affecting
& determining blood pressure.
Relationships between blood pressure, Cardiac Output, & Total Peripheral Resistance.

Recognize short, intermediate & long-term regulatory mechanisms of ABP. & different neural
& hormonal mechanisms that regulates ABP.
Baroreceptors regulatory mechanism of ABP. & Chemoreceptors regulatory mechanism of ABP.

Role of Kidney in long-term regulation of ABP.

 Types of Blood Pressure
“Depending on the nature of the blood vessels “

Arterial Blood Pressure Venous Blood Pressure Capillary Blood Pressure

Pressure Changes Throughout Systemic Circulation

• Blood flows down a pressure gradient. (the higher the pressure
• gradient the faster is the flow).
• Pressure is highest at the Heart (driving pressure), & decreases over
distance.
• Pressure decreases more than 90% from the Aorta to Vena cava.
• Greatest drop in pressure occurs in Arterioles (resistance vessels) which
regulate blood flow through tissues. Vasoconstriction and vasodilation both
happen to arterioles
• No large fluctuations of pressure in Capillaries & Veins.
• BP averages 120 mmHg in the Aorta & drops to 2 mmHg in the Right
Atrium. More difference in pressure ( pressure gradient)= more blood flow
Video recommended by doctor: click here Note : vaso = arterioles , veno = venules
 Blood pressure changes ٍExtra slide

From Guyton
Note at the far right side of the Figure the respective pressures in
the different parts of the pulmonary circulation. In the pulmonary
arteries, the pressure is pulsatile, just as in the aorta, but the
pressure is far less: pulmonary artery systolic pressure averages
about 25 mm Hg and diastolic pressure averages about 8 mm
Hg, with a mean pulmonary arterial pressure of only 16 mm Hg.
The mean pulmonary capillary pressure averages only 7 mm Hg.
Yet, the total blood flow through the lungs each minute is the
same as through the systemic circulation.the low pressures of the
pulmonary system are in accord with the needs of the lungs
because all that is required is to expose the blood in the
pulmonary capillaries to oxygen and other gases in the pulmonary
alveoli.
Explanation:
LV BP = 120/2
AORTIC BP=120/80 Blood pressure in different parts of the circulatory system.
: ‫ﻟﯾﮫ ھذا اﻻﺧﺗﻼف‬
aorta ‫ و‬LV ‫ ﯾﻔﺗﺢ وﯾﺻﯾر اﻟـ‬aortic valve ‫ﻻن ﻋﻧد أﻋﻠﻰ ﻗﯾﻣﺔ ﻟﻼﻧﻘﺑﺎض‬

2 ‫ ﯾﻧزل اﻟﻰ ﻣﺎﯾوﺻل‬LV ‫ اﻟﺿﻐط داﺧل اﻟـ‬valve ‫ﻟﻛن ﻋﻧد اﻋﻠﻰ ﻗﯾﻣﺔ ﻟﻼﻧﺑﺳﺎط ﯾﻘﻔل‬
systemic circulation it’s not a ‫ ﻻن اﻟدم راﯾﺢ ﻟﻠـ‬80 ‫ ﻣﺎﯾﻘدر ﯾﻧزل اﻛﺛر ﻣن‬aorta ‫ﻟﻛن ﺑﺎﻟـ‬
closed chamber
 Arterial Blood pressure ( ABP )
Introduction:
• Arterial blood pressure (ABP) : the lateral pressure force exerted by the blood flow
on the arterial wall against any unit area of the vessel wall .P=F/A
• The pressure force of blood flow is created & determined by the pumping force of the
heart.
• Arterial blood pressure (ABP) is one of the most important vital signs. Why? Because
steady ABP = stable perfusion for tissues
• It is important to keep normal levels of blood pressure for proper blood flow to the
body’s organs & tissues.
• Standard units of BP: mmHg and sometimes cmH₂O (1mmHg = 1.36 cmH₂O) 1 ml of
mercury pressure= 1.36 centimeters of water pressure because the specific gravity of
mercury is 13.6 times that of water, and 1 centimeter is 10 times as great as 1
millimeter.
• Arteries are pulsatile. (because their wall is made of thick smooth muscle, it’s not
fixed)
 Arterial Blood pressure Measures

Systolic Blood Pressure: Maximum Diastolic Blood Pressure: Minimum

force exerted by the blood flow against any unit force exerted by the blood flow against any
area of the vessel wall during unit area of the vessel wall during
maximum contraction (systole) of the heart. maximum relaxation (diastole) of the heart.

Normal Arterial Blood Pressure Levels:

Normal Levels are
90–120 mmHg systolic
60–80 mmHg diastolic. (It doesn’t have a specific value cuz the arteries pulsatile )
❖ Both numbers are important to determine the state of the heart health
❖ Greater numbers than the ideal range indicate that the heart is working too hard to pump blood to
the rest of the body. Ideal is less than 120/80. At aorta, it’s 120/80.
 Pulse and Mean Arterial Pressures

❖ Arterial pressure is pulsatile, so a single value is used

to represent the overall driving pressure. This is called
the Mean Arterial pressure (MAP). Pulsatile means it have
muscle thickness makes it palpable; that’s why the ABP
fluctuates.
❖ Mean arterial pressure is a better indicator of
perfusion to the vital organs than systolic blood
pressure.
❖ It’s responsible for driving blood into the tissues
throughout the cardiac cycle.
 Example
Mean Arterial Blood Pressure= If a patient’s blood pressure is 83/50
mmHg, his MAP would be 61 mm Hg.
Diastolic Pressure + ⅓(Pulse Pressure)
MAP = 1/3 (SBP - DBP) + DBP = 1/3
Pulse Pressure =Systolic-Diastolic (83-50) + 50
= 1/3 (33) + 50
OR =11 + 50
MAP = Systolic BP + 2 (Diastolic BP) = 61 mm Hg
Another way:
3 MAP = SBP + 2 (DBP)/3
MAP= 83 +2 (50) /3
MAP = 83 +100/3
MAP = 61
 Range & Variations In Arterial BP Levels
Blood Pressure Category Systolic Diastolic

Normal <120 And <80

Elevated (prehypertension) 120-129 And <80 Value Old Guidelines New Guidelines

High Blood Pressure 130-139 Or 80-89 <120 normal normal

(Hypertension) Stage 1

120-129 high normal elevated blood

High Blood Pressure 140 or Or 90 or pressure
(Hypertension) Stage 2 Higher Higher
130-139 high normal stage 1
Hypertensive Crisis ( consult Higher And Higher hypertension
your doctor immediately) /or
than 180 than 120

140 or Higher hypertension stage 2

hypertension
 Sex: Male > Female , equal at
Temperature:ABP ( ) with Heat
menopause.up to age of 40 years males have
due to vasodilatation, & ( ) with higher atrial pressure Than women, become lower than
Cold due to vasoconstriction. women after age 50

Age:ABP rises with age,

Pregnancy: ABP ( ) due to ( elderly > children, due to
) in hemodynamics. atherosclerosis, diabetes, …

Physiological Body mass index: ABP

Sleep:ABP ( ) due to ( Factors Affecting rises with body size.
)venous return.
Arterial Blood
Pressure Emotions:ABP ( )due to
Race:(? dietary factors, or neural & hormonal factors.
stress) ‫ﻣﺎﻋرﻓوا وش اﻟﺳﺑب ﻟﺣد اﻟﺣﯾن‬

Exercise:( ) ABP due to

Gravity:ABP is higher in venous return.
lower limbs than upper limbs.
Hormones:Some hormones
like adrenaline, noradrenaline
& thyroid H ( ) BP.
Physiological Factors Affecting Arterial Blood Pressure: Age

From Guyton : A slight extra increase in systolic pressure usually occurs beyond the age of
60 years. his increase results from decreasing distensibility, or “hardening,” of the arteries,
which is often a result of atherosclerosis. The final effect is a higher systolic pressure with
considerable increase in pulse pressure, as previously explained. Note that the mean pressure
(solid green line) at all ages is nearer to the diastolic pressure than to the systolic pressure.
However, at very high heart rates, diastole comprises a smaller fraction of the cardiac cycle and
the mean arterial pressure is more closely approximated as the average of systolic and diastolic
pressures.
 Only in female slide Except the definition of CO

Factors Determining Arterial Blood Pressure(MAP)

team 436: If one of these factors are
Blood Pressure = Cardiac Output X Peripheral Resistance missing then there will be 1. Cardiac
Output (Flow) NO blood pressure.

1. Cardiac Output (Flow) 2. Peripheral Resistance 3. Blood Volume

The amount of blood pumped by each Depends on: Depends on:

ventricle in 1 minute.average: 4900-5000
Determined by :
1-stroke volume
2-heart rate
CO = Stroke volume(SV) x Heart
rate(HR)
Note that Any increase in the
(SV)or (HR)will increase the CO
which will eventually increase the
arterial blood pressure
1- size of the blood vessel (r) 1- Fluid intake
2- blood viscosity/thickness (η) 2- Fluid loss
3- length of blood vessels (L) Note that any increase the Blood
remains constant so we can ignore it volume will eventually increase the
arterial blood pressure
Note that any increase in
Peripheral Resistance will
eventually increase the arterial
blood pressure

Final note : ‫أي ﺗﻐﯾﯾر ﻓﻲ اﻟﻌواﻣل اﻟﻠﻲ ﺗؤﺛر ﻋﻠﻰ اﻟﻌواﻣل اﻟﻣؤﺛرة ﻋﻠﻰ ﺿﻐط اﻟدم راح ﯾﺄﺛر ﻋﻠﻰ ﺿﻐط اﻟدم‬we will discuss that in the next slides
 Only in female slide
Regulation of Cardiac Output
Cardiac Output= Stroke Volume x Heart Rate

CO is regulated by: i) Regulation of Stroke Volume (SV)

i) Regulation of stroke volume (SV
) ii) Regulation of Heart Rate Stroke volume : The Amount of blood ejected from each ventricle with each
contraction. 70-80 ml/beat.
Stroke Volume = EDV – ESV
Stroke volume (SV) is regulated by 3 variables:
EDV: Is the volume of blood in the
ventricle at the end of diastole.
110-130 mL 1)End Diastolic Volume: Affect the (EDV)
ESV : Is the volume of blood remains Affected by the preload (venous return).
in the ventricle at the end of systole.
40-60 mL 2)Contractility (Strength of contraction):Affect the (ESV)
Affected by Starling’s law & sympathetic innervation.
End diastolic volume ≠ preload
preload (VR) is all the blood returning to the
heart. 3) Total Peripheral Resistance Affected by the (Afterload): Affect the(ESV)
End diastolic volume is the amount of blood Affected by size length of blood vessel. Thickness (viscosity) of blood.
that fully fills the ventricle up.
1. Factors Affecting End-Diastolic Volume 2. Factors Affecting End-Systolic Volume

End-diastolic pressure is affected by the preload a)Cardiac contractility:

(venous return) which is affected by:

Only in female slide

Intrinsically affected by: Frank Starling’s law of the
1. Blood volume. heart, which is & affected by the End Diastolic
Volume (EDV). [Frank Starling’s law states that the
2. Pressure gradient
force of contraction depends on theinitial length of
3. Gravity. the muscle].
Extrinsically affected by sympathetic stimulation,
4. Veno-constriction: caused by sympathetic
hormones and drugs.
nervous system. ↑↑ contractility → ↑↑ SV → ↓↓ ESV
↓↓ contractility → ↓↓ SV → ↑↑ ESV
5. Presence of valves in the large veins.
b)Total Peripheral Resistance (Afterload=MAP):
6. Skeletal muscles pump.
In response to all regulatory mechanisms
7. Respiratory activity (Deep inspiration venous
↑↑ Peripheral Resistance (Vasoconstriction)→ ↓↓
return). Flow → ↓↓ SV → ↑↑ ESV
↓↓Peripheral resistance (Vasodilatation) →
↑↑ Flow → ↑↑ SV → ↓↓ ESV
 2) Regulation of Heart Rate

Heart rate: The number of contractions of the ventricles each minute.

Only in female slide Except the definition of HR

Normal heart rate (HR) = 60-100 beats/min
If > 100 beats/min → Tachycardia
If < 60 beats/min → Bradycardia
Heart Rate is regulated by:

1. Autonomic Nervous System. 2. Hormones/Drugs

Sympathetic nerves → increase HR

Epinephrine & thyroxine→ increase HR.
Parasympathetic nerves (vagus nerve)→slow HR.
HR is regulated by autonomic nervous system through cardiac
Decrease blood calcium→ decreases HR.
control centers in medulla oblongata in the brain stem:

1- Cardiac-accelerator Center (Vasomotor center) Sympathetic

nerve fibers Function : Sympathetic, drugs, and parasympathetic
1. increase HR affect HR
2. increase cardiac contractility (ventricular contractility not atrial since
Only sympathetic and drugs affect
ventricles are the actual
pumps). 3. vasoconstriction 4. adrenal medulla release of adrenaline and contractility (parasympathetic has no
noradrenaline effect on contractility)
2- Cardiac-inhibitory Center Parasympathetic nerve fibers
Function:
1. Decrease HR (ONLY one function)
**note that they never function at the same time; one is stimulated and the other is
inhibited (not blocked).
 Regulation of Cardiac Output

Peripheral Resistance (Afterload)

(Mean arterial blood pressure)

Cardiac Output = Stroke Volume X Heart Rate

Cardiac output: output of ventricle per minute

5 L/min ( av. 5-6 L/min ) End diastolic Strength of
Stroke volume: output of ventricles per beat volume (EDV) Contraction
Parasympathetic n
70 ml/beat ( av. 70-80 ml / beat )
Heart Rate : beats / minute
70-75 beats / min ( av. 60 -100 beats / min ) Hormones/Drugs
Intrinsic
Starling’s law of the heart – the more the cardiac Stretch
Frank -
Sympathetic n
muscle is stretched, the stronger the contraction Starling Extrinsic
 Peripheral Resistance (PR):
Affecting Factors

Only in female slide

Vascular Resistance (R) is the tendency of the
vascular system to oppose the flow (Q).
Vascular Resistance (R)is affected by the pressure ∆P
difference (∆P) & the blood flow (Q) R=
Vascular Resistance (R)is affected directly by the Q
pressure difference (∆P).
Vascular Resistance (R)is affected inversely by the
amount of blood flow (Q).
 Total Peripheral Resistance (TPR):
Total Peripheral Resistance (TPR) is higher in the systemic circulation than
the pulmonary circulation.

Systemic Circulation
TPR = Aortic pressure - RAP
Flow
120 - 2 mmhg
TPR =
83.3 ml/sec ( 5 L/min)
TPR = 1.2 (PRU’s) 1.41
∆P
Pulmonary Circulation R=
Q
Pulmonary R = Pulmonary Pressure - LAP
Flow TPR= Total Peripheral
15 - 3 mmHg Resistance; PulR=
Pulmonary R=
83.3 ml/sec (5 L/min) Pulmonary Resistance;
RAP= Right Atrial Pressure;
LAP= Left Atrial Pressure;
PRU= Peripheral
Pulmonary R = 0.12 (PRU’s) 0.14 Resistance 31
Units.
 Blood Flow (we will discuss resistance here)

Only in female slide

Blood flow (Q) is the amount of blood moving through a vessel in a given
time period.
Generally, blood flow equals to the Cardiac Output (CO).
Blood flow has 2 equations:
From guytone : the blood flow to body
2. Poiseuille’s Law: according to tissue’s needs, tissue needs
1. more blood flow when they are active.
∆P Most tissues “autoregulate” their own
(Pi-Po)πr4
Q= Q= blood flow ’permits blood flow from one
tissue to be regulated independently of
R 8ηL flow to another tissue’ .

The blood flow (Q) is affected by the pressure difference (∆P) & the resistance (R). Flow and Poiseuille’s Law
(Pi-Po)=∆P: difference in pressure (direct relationship) R: Resistance Fluid Flow (Q) through cylindrical tubes.
. r: radius (direct). ƞ: Viscosity (inverse). L: Length (inverse). Flow ↓ when resistance ↑.
Flow resistance ↓ when vessel diameter ↑.
 Pressure Difference Resistance

Only in female slide

Pressure difference: the driving pressure in a Resistance: tendency of vascular system to
vascular system (i.e. driving pressure/pressure oppose flow.
gradient). Pressure difference is directly Resistance is Inversely proportional to the flow
proportional to the flow (Flow = 1/R)
Blood flows down a pressure gradient According to Poiseuille’s Law R = 8ηL/πr4,
Absolute value of pressure is not important to so Resistance is influenced by:
flow, but the difference in pressure (DP or 1. Radius of the tube (r)
gradient) is important to determining flow. 2. Viscosity of the blood (η)
3. Length of the tube (L)

In a normal human, length of the vascular system

is fixed, so blood viscosity & radius of the blood
vessels have the largest effects on the resistance.

From guytone : pressure between the two ends of the vessel that
provides the driving force for flow
pressure gradient is much lower in pulmonary circulation than that
in the systemic circulation but the blood flow is the same .
 Effect of Radius (r) & Pressure on Flow

Only in female slide

Radius with flow Radius with pressure
Directly proportional to flow. Inversely proportional to pressure
Vascular tone - effects
❖ Increased tone in a segment of blood vessel e.g increased
arteriolar tone.
❖ Decreased radius of arteriole.
❖ Greatly increased blood across the arteriole
❖ The effect on blood volume
- Increased upstream (in artery).
- Decreased downstream (in capillaries).
 Factors Affecting Vessel Diameter: Radius (r)

Vasodilator Agents Vasoconstrictor Agents

Radius of vessel ⬆ = blood flow ⬆
& the peripheral resistance and the
CO2 & other Oxygen (O2) Endothelin-1
pressure decreased
Histamine
metabolites

Prostacyclin Vasopressin
Nitric Oxide (NO) Thromboxane A2
(PGI2) (also called ADH)

Atrial Natriuretic
Peptide (ANP)
[H+] Angiotensin II Norepinephrine

β 2 R. α 1 R.
Cold
 Effect of Viscosity & Length on Flow

Only in female slide

Effect of Viscosity (η) on flow Effect of Length (L) on flow

❖ Blood viscosity is the thickness & stickiness of ❖ Length is inversely proportional to the flow.
the blood
❖ Human blood is five times more viscous than N.B. In a normal human, length of the vascular
distilled water system is fixed (cannot change).
❖ It is an important factor that determines the
resistance of blood to flow.
❖ Viscosity of the whole blood is mainly due to
cells, & that of plasma is due to plasma proteins.
❖ Viscosity is inversely proportional to the flow.

viscosity increases as plasma decreases as a result

of sweating,diarrhea,vomiting.
 Flow (Q) and Cross-Sectional Area

V=Q/A
Q= Flow
A= cross section
V= velocity

As diameter of vessels decreases

The total cross-sectional area
increases
Velocity of blood flow decreases
Explanation:
A single Aorta has a cross section of 2.5cm^2 How many aoera is there at the same level?
only one so 2.5^2 (1)= 2.5^1
a single capillary has a cross section of say 0.3^2 But How many capillaries are there at the same level? 10000
so 03^2 (10000)= 30000^2 and that’s why capillaries has higher cross sectional area than aorta because there
are so many of them which is good we need it to be slower because that’s where exchange occure
Note: numbers are not accurate I was only trying to make a point
 Compliance (C) of Blood Vessels:
• Compliance = Distensibility.
‫ﺻﻔﺔ اﻟﻣطﺎطﯾﺔ؛ ﻗَﺎ ِﺑﻠِ ﱠﯾ ُﺔ اﻟ ﱠﺗ َﻣ ﱡد ِد‬
• Compliance is the volume (V) of blood that the
vessel can hold at a given
pressure (P).

• Venous system has a large compliance & acts as

a blood reservoir (high
volume & low pressure).
You’re half way through, keep going!
 Regulation of Arterial Blood Pressure
In order to regulate the blood pressure, determining factors should be
regulated:
• Cardiac output (Flow.)
• Peripheral Resistance.
• Blood volume.

Blood Pressure = Cardiac Output X Peripheral Resistance

 Mechanisms Regulating Mean Arterial Blood Pressure
Naturally- mediated Long term (slow response)
Intermediate
Fast response (short-term) Endocrine mechanism

Concerned in regulating CO and PR Angiotensin vasoconstriction Aldosteron system (excitatory)

1. Baroreceptor Reflex (excitatory or

ADH Vasoconstriction system Vasopressin (excitatory)
inhibitory)

Fluid shift mechanism

2. Chemoreceptor reflex (excitatory) Natriuretic peptide (Inhibitory)
(Excitatory + inhibitory)

3. CNS ischemic response (excitatory)

FAST

Other vasomotor reflexes: Stress-Relaxation mechanism

Erythropoietin ( Excitatory)
● atrial stretch (Inhibitory) (Inhibitory)
● Thermoreceptors (inhibitory &
excitatory)
● Pulmonary receptor (Excitatory)
 Rapidly Acting Control Mechanisms
● Acts Within sec/min.
● Concerned in regulating the Cardiac Output (CO) & the
Peripheral Resistance (PR).
● Reflex mechanisms act through the autonomic nervous
system:
Centers in Medulla Oblongata:
• Cardio-Acceleratory (CAC) or Vasomotor
Center (VMC) → Sympathetic nervous system
• Cardio-Inhibitory Center (CIC) → Parasympathetic nervous
system.
 Autonomic Nervous System Stimulation

Heart ↑HR ↑Contractility

Sympathetic
CAC/VMC nervous system
activation Arterioles Vasoconstriction

Venules Vasoconstriction
Medulla Oblongata

Parasympathetic
CIC nervous system Heart ↓HR
activation

CAC= Cardioacceleratory center; VMC= Vasomotor center; CIC= Cardiac inhibitory

center.
 Baroreceptor Reflex
• Baroreceptors are Mechano-stretch receptors.
• Located in the wall of carotid sinus & aortic arch.
• Stimulated in response to blood pressure changes
• Fast & Neurally mediated.
• Stimulation of Baroreceptors will send sensory signals through
Glossopharyngeal nerve fibers to the required centers in

medulla oblongata.

• Provide powerful moment-to-moment control of arterial blood pressure.

Baroreceptor Reflex
 Key: Stimulus - Receptor - Afferent ↓ Arterial Blood pressure/MAP
pathway - Integrating center - Efferent
pathway - Effector - Tissue response -
Systemic response

↓ Firing of baroreceptors in
carotid arteries and aorta

Sensory neurons

Reflex via cardiovascular control ↓ Parasympathetic output

↑ Sympathetic output center in medulla oblongata (vagal activity)
Less NE released Less ACh on
muscarinic
receptor
b1 receptor
a receptor

Arteriolar smooth muscle ventricular myocardium SA node

Vasocontraction ↑ Force of contraction ↑ Heart rate

↑ Peripheral resistance ↑ Cardiac output

Negative
feedback ↑ Arterial blood pressure/MAP
 Baroreceptor Reflex Mechanism During Changes in Body
Posture
● On immediate standing, Arterial Pressure in the head & upper parts of the body tends

to fall, which may cause loss of consciousness.

● Falling pressure will elicit an immediate reflex at the Baroreceptors, resulting in strong

sympathetic discharge throughout the body.

● This immediate reflex mechanism minimizes the drop in the arterial pressure that

occured in the head & upper parts of the body

 Rapidly Acting :
2- Chemoreceptors Reflex
● Closely associated with the baroreceptor pressure control system.
● Chemoreceptor reflex operates in much same way as the baroreceptor reflex, EXCEPT that chemoreceptors are
chemo-sensitive cells instead of stretch receptors.
● Chemoreceptors have high blood flow (1200 ml/min/g tissue), which make it easy for these cells to detect changes
in O2, CO2, & 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.
● Their 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.
 FEMALE SLIDE
Types of Respiratory
Chemoreceptors

Central Chemoreceptors Peripheral (arterial) Chemoreceptors

- Sensory receptors located in carotid &

- Sensory receptors located in the
medulla itself.
- Very sensitive to CO2 excess (↑)
& (↓) pH in medulla
aortic bodies
- Sensitive to O2 lack (↓), CO2 (↑or↓), &
pH (↑or↓)
- Chemoreceptors’ stimulation excite
nerve fibers, along with baroreceptor
fibers.
- They are stimulated when the MAPis
lower than 60 mmHg.
 Rapidly Acting: 2-Chemoreceptors Reflex
Chemoreceptor reflexes usually act to Peripheral chemoreceptors Reflex
increase BP

FEMALE SLIDE
Haemorrhage ↓ BP

Hypoxia

+ Peripheral Chemoreceptors

++ Vasomotor Center = Cardioinhibitory Center

(VMC) (CIC)

+ Sympathetic nerve fibers = Parasympathetic

+ Adrenal nerve fibers
medulla
Vasoconstriction &
↑Total ↑ Cardiac Output ↑ Heart Rate
peripheral resistance p.s.= means no change, + means
(TPR)
(CO) (HR)
increases
 Rapidly Acting:3-CNS Ischemic Response
“Last Ditch Stand” Pressure Control Mechanism

It is not one of the normal regulatory mechanisms of ABP. It operates principally as an

01 emergency pressure control system to prevent further decrease in arterial pressure
whenever blood flow to the brain.

It’s one of the most powerful activators of the sympathetic vasomotor (vasoconstrictor system)
02 nervous control areas in medulla oblongata.

03 It acts rapidly and very powerfully.

It acts whenever blood flow to the brain ↓ dangerously close to the lethal level (MAP < 20mmHg
04 ) → cerebral ischemia of vasomotor center → strong excitation of vasomotor center due to
accumulation of local CO2 & lactic acid, in order to prevent further decrease in arterial pressure
(MAP) → strong vasoconstriction of blood vessels including the kidney arterioles.
 Rapidly Acting:Other Vasomotor Reflexes
1) Atrial stretch receptor reflex:
Receptors in large veins close to heart, walls of the atria (response of blood volume).
↑ Venous Return (increase blood volume) → ++ stretch atria & activate atrial stretch receptors → sensory
afferent nerves to medulla → inhibiting the cardiovascular center → reflex decrease in blood volume & ↓
ABP 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.
 Rapidly Acting:Other Vasomotor Reflexes

2) Thermo-receptors: (in skin/hypothalamus)

❖ Exposure to heat → vasodilatation. (team 438: Allows fluid to exit and absorb the heat).
❖ Exposure to cold → vasoconstriction. (team 438 : Allows the heat to be trapped in the
system).
3) Pulmonary receptors:
❖ Lung inflation → vasoconstriction
Hormonally- Mediated Regulation of ABP
Slow Response (Long- Term)
 Long- Term (Slow Response) Regulation
• Hormonally mediated.
• Takes few hours to being showing significant response.
• Concerned in regulating blood volume.
Mainly Renal (Acts if BP is too low):
1. Renin-Angiotensin-Aldosterone System
2. Vasopressin/Anti-Diuretic hormone (ADH)
- Hypovolemia & dehydration stimulates
Hypothalamic Osmoreceptors
- ADH will be released from posterior pituitary
gland:
- Promotes water reabsorption at kidney tubules
leading to↑blood volume.
- Causes vasoconstriction, in order to ↑ ABP.
- Thirst stimulation.
- Usually, when secreted aldosterone is secreted.
Others:
Long-term
Regulation
3. Low-pressure volume receptors:
Atrial Natriuretic Peptide Mechanism(weaker
effect than RAAS & ADH)
- ANP is a hormone released from cardiac muscle
cells (wall of right atrium) as a response to an
increase in ABP in order to
decrease the blood volume.
- Simulates an ↑ in urinary production, causing a ↓ in
blood volume & blood pressure.
4. Erythropoietin(EPO)
- Secreted by the kidneys when blood volume is too low.
- Leads to RBCs formation → ↑ blood volume.
 1. Renin-Angiotensin Aldosterone
System
↓ Renal blood flow and/or ↓Na+

Angiotensinogen( Plasma protein)

++ Juxtaglomerular
apparatus of kidneys
(considered volume Renin
receptors)
Angiotensin I
Angiotensin
converting
enzymes (ACEs)

Adrenal Cortex
Aldosterone Corticosterone Angiotensin II (powerful
vasoconstrictor + Thirst stimulation)

(Na+& Water Hypothalamus

retention) At
kidney tubules
Angiotensin III
Thirst and drinking (powerful
Result: Elevated blood pressure vasoconstrictor)
 2. Anti-Diuretic Hormone (ADH), or
Vasopressin
• Hypovolemia & dehydration stimulates Hypothalamic Osmoreceptors.
• ADH will be released from posterior Pituitary gland:

Promotes Water reabsorption at kidney tubules to ↑ blood volume.

Causes Vasoconstriction, in order to ↑ ABP.

• Thirst stimulation.
• Usually, when secreted Aldosterone is secreted.
 3 . Low-pressure volume receptors
● Atrial Natriuretic Peptide (ANP) hormone:
● Hormone released from cardiac muscle cells (wall of Right Atrium)

as a response to an increase in ABP in order to decrease the blood volume.

• Simulates an ↑ in urinary production, causing a ↓ in blood volume & blood pressure.

4 . Erythropoietin (EPO)
• Secreted by the kidneys when blood volume is too low.
• Acts in the bone marrow & leads to formation of Red blood cells
( RBCs) → to ↑ blood volume.
 Intermediate Mechanisms Regulating ABP
• Activated within 30 min to several hrs
• During this time, the nervous mechanisms usually become less & less effective.

1 3

Renin-angiotensin vasoconstriction ADH vasoconstriction

mechanism (system). mechanism (system)
2
Fluid(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
4
Stress-relaxation of the vasculature
- Adjustment of blood vessel smooth muscle
to respond to changes in blood volume.
- When pressure in blood vessels becomes
too high, they become stretched & keep on
stretching more & more for minutes or hours;
resulting in fall of pressure in the vessels
toward normal.
- This continuing stretch of the vessels can
serve as an
intermediate-term pressure “buffer.”
 MALE SLIDE
Renal Body fluid control mechanism
Credit: team439
 MALE SLIDE
Renal Body fluid control mechanism
Credit: team439
 FEMALE SLIDE
Control mechanisms at different time
intervals after onset of a disturbance
to the arterial pressure:
 Team Leaders
QBank
Team
Rand aldajani Nawaf Alshehri

Sub Leader
Samiah AlQutub

Team Members
Arwa Awwad Ftoon Alzahrani