Course 12

Arterial blood pressure

I.Definitions and normal values

Arterial blood pressure is defined as the lateral pressure exerted by the column of blood on wall
of arteries.
The pressure is exerted when blood flows through the arteries. Generally, the term ‘blood
pressure’ refers to arterial blood pressure. Actually, blood pressure means the force exerted by the blood
against any unit area of the vessel wall. When we says that the pressure in a vessel is 50 mm Hg, this
means that the force exerted is sufficient to push a column of mercury against gravity up to a level 50
millimeters high. If the pressure is 100 mm Hg, it will push the column of mercury up to 100 millimeters

Arterial blood pressure is expressed in four different terms:

1. Systolic blood pressure
2. Diastolic blood pressure
3. Pulse pressure
4. Mean arterial blood pressure.
1. SYSTOLIC BLOOD PRESSURE
Systolic blood pressure (systolic pressure) is defined as the maximum pressure exerted in the
arteries walls during systole of heart.
Normal systolic pressure: 120 mm Hg (110 mm Hg to 140 mm Hg).
2. DIASTOLIC BLOOD PRESSURE
Diastolic blood pressure (diastolic pressure) is defined as the minimum pressure exerted in the
arteries walls during diastole of heart.
Normal diastolic pressure: 80 mm Hg (60 mm Hg to 80 mm Hg).
3. PULSE PRESSURE
Pulse pressure is the difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
4. MEAN ARTERIAL BLOOD PRESSURE
Mean arterial blood pressure is the average pressure existing in the arteries. It is not the
arithmetic mean of systolic and diastolic pressures. It is the diastolic pressure plus one third of pulse
pressure. To determine the mean pressure, diastolic pressure is considered than the systolic pressure. It
is because, the diastolic period of cardiac cycle is longer (0.53 second) than the systolic period (0.27
second).
Normal mean arterial pressure: 93 mm Hg (80 + 13= 93).

Formula to calculate mean arterial blood pressure:

Mean arterial blood pressure = Diastolic pressure + 1/3 of pulse pressure = 80 + 40/3 = 93.3 mm Hg

II . Variations
Blood pressure is altered in physiological and pathological conditions. Systolic pressure depend
on a lot factors an can have variations easily and quickly and its variation occurs in a wider range.
Diastolic pressure variation occurs in a narrow range and are not so easily and quickly.

A. PHYSIOLOGICAL VARIATIONS
1. Age
Arterial blood pressure increases as age advances.
Systolic pressure in different age:
Newborn : 70 mm Hg
After 1 month : 85 mm Hg
After 6 month : 90 mm Hg
After 1 year : 95 mm Hg
At puberty : 120 mm Hg
 At 50 years : 140 mm Hg
At 70 years : 160 mm Hg
At 80 years : 180 mm Hg
Diastolic pressure in different age
Newborn : 40 mm Hg
After 1 month : 45 mm Hg
After 6 month : 50 mm Hg
After 1 year : 55 mm Hg
At puberty : 80 mm Hg
At 50 years : 85 mm Hg
At 70 years : 90 mm Hg
At 80 years : 95 mm Hg
2. Sex
In females, up to the period of menopause, arterial pressure is 5 mm Hg, less than in males of same age.
After menopause, the pressure in females becomes equal to that in males of same age.
3. Body Built
Pressure is more in obese persons than normal weight persons.
4. Diurnal Variation
In early morning, the pressure is slightly low. It gradually increases and reaches the maximum at noon. It
becomes low in evening.
5. After Meals
Arterial blood pressure is increased for few hours after meals due to increase in cardiac output.
6. During Sleep
Usually, the pressure is reduced up to 15 to 20 mm Hg during deep sleep but can increases slightly in
association with dreams.
7. Emotional Conditions
During excitement or anxiety, the blood pressure is increased due to release of adrenaline.
8. After Exercise
After moderate exercise, systolic pressure increases by 20 to 30 mm Hg above the basal level due to
increase in rate and force of contraction of the heart and stroke volume. Normally, diastolic pressure is
not affected by moderate exercise. It is because, the diastolic pressure depends upon peripheral
resistance, which is not altered by moderate exercise.
After intense muscular exercise, systolic pressure rises by 40 to 50 mm Hg above the basal level. But,the
diastolic pressure reduces because the peripheral resistance decreases.

3. Determinants of arterial blood pressure – factors maintaining arterial blood pressure

Some factors are necessary to maintain normal blood pressure. These factors are called local factors,
mechanical factors or determinants of blood pressure. They can be divided in central factors and
peripheral factors

A. Central factors, which are related to the heart performance :

1. Cardiac output
2. Heart rate

B. Peripheral factors, which are related to blood and blood vessels:

1. Peripheral resistance
2. Blood volume
3. Venous return
4. Elasticity of blood vessels
5. Velocity of blood flow
6. Diameter of blood vessels
7. Viscosity of blood.
 A. CENTRAL FACTORS

1. Cardiac Output
Systolic pressure is directly proportional to cardiac output. Whenever the cardiac output
increases, the systolic pressure is increased and when cardiac output is decrease , the systolic pressure
is reduced. Cardiac output increases in muscular exercise, emotional conditions, etc and decrease in
condition like myocardial infarction , when the myocardial contraction capacity is affected resulting in fall
in systolic pressure.
2. Heart Rate
Moderate changes in heart rate do not affect arterial blood pressure much. However, marked
alteration in the heart rate affects the blood pressure by altering cardiac output .
3. Stoke volume
Depend on the venous return

B. PERIPHERAL FACTORS

1. Peripheral Resistance
Peripheral resistance is the important factor, which maintains diastolic pressure. Diastolic
pressure is directly proportional to peripheral resistance.The arterioles are involved , they are called
the resistant vessels. When peripheral resistance increases, diastolic pressure is increased and when
peripheral resistance decreases, the diastolic pressure is decreased.
2. Blood Volume
Blood pressure is directly proportional to blood volume.Blood volume maintains the blood
pressure through the venous return and cardiac output. If the blood volume increases, there is an
increase in venous return and cardiac output, resulting in elevation of blood pressure.
3. Venous Return
Blood pressure is directly proportional to venous return. When venous return increases, there is
an increase in ventricular filling and cardiac output, resulting in elevation of arterial blood pressure.
4. Elasticity of Blood Vessels
Blood pressure is inversely proportional to the elasticity of blood vessels. Due to elastic
property, the blood vessels are opposing to stretch and are able to maintain the pressure. When the
elastic property is lost, the blood vessels become rigid due to the arteriosclerosis and pressure
increases as in old age.
5. Velocity of Blood Flow
Pressure in a blood vessel is directly proportional to the velocity of blood flow. If the velocity of
blood flow increases, the resistance also is increased and due to that the pressure is increased.
6. Diameter of Blood Vessels
Arterial blood pressure is inversely proportional to the diameter of blood vessel. If the diameter
decreases, the peripheral resistance increases, leading to increase in the pressure.
7. Viscosity of Blood
Arterial blood pressure is directly proportional to the viscosity of blood. When viscosity of blood
increases, the frictional resistance is increased and this increases the pressure.

The last factors involvement in the peripheral resistance is explained by the Poiseuille-Hagen equation.

R is the resistance , r is the inner radius of the tube, l is its length, and η is the viscosity.
4. Regulation of arterial blood pressure

Body has four regulatory mechanisms to maintain the blood pressure within normal limits
A. Nervous mechanism or short term regulatory mechanism
B. Renal mechanism or long term regulatory mechanism
C. Hormonal mechanism
D. Local mechanism

A. Nervous mechanism for regulation of blood pressure or Short-term regulation mechanism

Nervous regulation is the most rapid among all the mechanisms involved in the regulation of arterial
blood pressure.
When the pressure is altered, nervous system brings the pressure back to normal within few minutes.
Although nervous mechanism is quick in action, it operates only for a short period and then it adapts
to the new pressure. Hence, it is called short term regulation mechanism. The nervous mechanism
regulating the arterial blood pressure operates through the autonomous nervos system.
Vasomotor System
Vasomotor system includes three components:
1. Vasomotor center
2. Vasoconstrictor fibers
3. Vasodilator fibers.
„ Vasomotor center
Vasomotor center is bilaterally situated in the reticular formation of medulla oblongata and the lower part
of the pons.
Vasomotor center consists of three areas:
i. Vasoconstrictor area
ii. Vasodilator area
iii. Sensory area.
i. Vasoconstrictor Area
Vasoconstrictor area is also called the pressor area. It forms the lateral portion of vasomotor center.
Vasoconstrictor area sends impulses to blood vessels through sympathetic vasoconstrictor fibers. So, the
stimulation of this area causes vasoconstriction and rise in arterial blood pressure. This area is also
concerned
with acceleration of heart rate.
ii. Vasodilator Area
Vasodilator area is otherwise called depressor area. It forms the medial portion of vasomotor center.
This area suppresses the vasoconstrictor area and causes vasodilatation. It is also concerned with
cardioinhibition
iii. Sensory Area
Sensory area is in the nucleus of tractus solitarius, which is situated in posterolateral part of medulla and
pons. This area receives sensory impulses via glossopharyngeal and vagal nerves from the periphery,
particularly from the baroreceptors. Sensory area in turn, controls the vasoconstrictor and vasodilator
areas.

Vasoconstrictor fibers
Vasoconstrictor fibers belong to the sympathetic division of autonomic nervous system. These fibers
cause vasoconstriction by the release of neurotransmitter substance, noradrenaline. Noradrenaline acts
through alpha receptors of smooth muscle fibers in blood vessels.Vasoconstrictor fibers play major role
than the vasodilator fibers in the regulation of blood pressure.
Vasomotor Tone
Vasomotor tone is the continuous discharge of impulses from vasoconstrictor center through the
vasoconstrictor fibers. Vasomotor tone plays an important role in regulating the pressure by producing a
constant partialstate of constriction of the blood vessels. Thus, the arterial blood pressure is directly
proportional to the vasomotor tone. Vasomotor tone is also called sympathetic vasoconstrictor tone or
sympathetic tone.
Vasodilator fibers
Vasodilator fibers are of three types:
i. Parasympathetic vasodilator fibers
ii. Sympathetic vasodilator fibers
iii. Antidromic vasodilator fibers.
i. Parasympathetic Vasodilator Fibers
Parasympathetic vasodilator fibers cause dilatation of blood vessels by releasing acetylcholine.
ii. Sympathetic Vasodilator Fibers
Some of the sympathetic fibers cause vasodilatation in certain areas, by secreting acetylcholine. Such
fibers are called sympathetic vasodilator or sympathetic cholinergic fibers. Sympathetic cholinergic
fibers,which supply the blood vessels of skeletal muscles, are important in increasing the blood flow to
muscles by vasodilatation, during conditions like exercise. Sympathetic cholinergic vasodilator fibers form
the important part of vasomotor system. Signals for the vasodilator fibers are generated in cerebral
cortex.Signals are relayed through the fibers from cerebral cortex to lateral gray horn of the spinal cord
via hypothalamus, midbrain and medulla. In the spinal cord, these impulses activate the preganglionic
sympathetic fibers. These fibers in turn, activate the postganglionic fibers. Postganglionic fibers cause
dilatation of blood vessels by secreting acetylcholine.
iii. Antidromic Vasodilator Fibers
Normally, the impulses produced by a cutaneous receptor (like pain receptor) pass through sensory nerve
fibers. But, some of these impulses pass through the other branches of the axon in the opposite direction
and reach the blood vessels supplied by these branches. These impulses now dilate the blood vessels. It
is called It is called the antidromic or axon reflex and the nerve fibers are called antidromic vasodilator
fiber

Mechanism of action of vasomotor center in the regulation of blood pressure

Vasomotor center regulates the arterial blood pressure by causing vasoconstriction or vasodilatation.
However,its actions depend upon the impulses it receives from other structures such as baroreceptors,
chemoreceptors,higher centers and respiratory centers. Among these structures, baroreceptors and
chemoreceptors play a major role in the short term regulation of blood pressure.
1. Baroreceptor Mechanism
Baroreceptors are the receptors, which react at blood pressure change. Baroreceptors are also called
pressoreceptors.
Baroreceptors are situated in the carotid sinus and wall of the aorta. When the blood pressure
increase baroreceptors are activated and send stimulatory impulses to nucleus of tractus solitarius
through glossopharyngeal and vagus nerves. From here due to the nucleus of tractus solitaries tract
impulses goes on both vasoconstrictor area and vasodilator areas of vasomotor center. It inhibits the
vasoconstrictor area and excites the vasodilator area.
Inhibition of vasoconstrictor area reduces vasomotor tone. Reduction in vasomotor tone causes
vasodilatation, resulting in decreased peripheral resistance. Simultaneous excitation of vasodilator center
increases vagal tone. This decreases the rate and force of contraction of heart, leading to reduction in
cardiac output. These two mechanism decreased peripheral resistance and reduced cardiac output and
bring the arterial blood pressure back to normal level.
.When blood pressure decreases the pressure in carotid sinus also decrease . This causes inactivation of
baroreceptors. Now, there is no inhibition of vasoconstrictor center or excitation of vasodilator center.
Therefore, the blood pressure rises.
Information regarding blood pressure within the range of 50 to 200 mm Hg (mean arterial pressure)
reaches the vasomotor center through the carotid baroreceptors.
Information about the blood pressure range of 100 to 200 mm Hg are detected thought aortic
baroreceptors.
Both carotid and aortic baroreceptors are stimulated by the rising of the pressure and their response
depends upon the rate of increase in the blood pressure.
Since the baroreceptor mechanism acts against the rise of the arterial blood pressure, it is called
pressure buffer mechanism or system and the nerves from baroreceptors mechanism are called the
buffer nerves.
2. Chemoreceptor Mechanism
Chemoreceptors are the receptors giving response to change in chemical constituents of blood.
Peripheral chemoreceptors influence the vasomotor center. Peripheral chemoreceptors are situated in the
carotid body and aortic body . Peripheral chemoreceptors are sensitive to lack of oxygen, excess of
carbon dioxide and hydrogen ion concentration in blood. Whenever blood pressure decreases, blood flow
to chemoreceptors decreases ,resulting in oxygen concentration decrease and excess of carbon dioxide
and hydrogen ion. These fact will stimulated the chemoreceptors, which send impulses to stimulate
vasoconstrictor center. Blood pressure rises and blood flow increases.
Chemoreceptors play a major role in maintaining respiration rather than blood pressure.
3. Sinoaortic mechanism
Mechanism of action of baroreceptors and chemoreceptors in carotid and aortic region constitute
sinoaortic mechanism. Nerves supplying the baroreceptors and chemoreceptors are called buffer nerves
because these nerves regulate the heart rate blood pressure and respiration.
4. Higher Centers
Vasomotor center is also controlled by the impulses from the two higher centers in the brain.
i. Cerebral cortex
Area 13 in cerebral cortex is concerned with emotional reactions. During emotional conditions, this area
sends impulses to vasomotor center. Vasomotor center is activated, the vasomotor tone is increased and
the pressure rises.
ii. Hypothalamus
Stimulation of posterior and lateral nuclei of hypothalamus causes vasoconstriction and increase in blood
pressure. Stimulation of preoptic area causes vasodilatation and decrease in blood pressure. Impulses
from hypothalamus are mediated via vasomotor center.
5. Respiratory Centers
During the beginning of expiration, arterial blood pressure increases slightly, i.e. by 4 to 6 mm Hg. It
decreases during later part of expiration and during inspiration because of two factors:
i. Radiation of impulses from respiratory centers towards vasomotor center at different phases of
respiratory cycle
ii. Pressure changes in thoracic cavity, leading to alteration of venous return and cardiac output.

B. Renal mechanism for regulation of blood pressure – Long-term regulation

Kidneys play an important role in the long term regulation of arterial blood pressure. When blood pressure
alters slowly in several days/months/years, the nervous mechanism adapts to the altered pressure and
looses the sensitivity for the changes. It cannot regulate the pressure any more. In such conditions, the
renal mechanism operates efficiently to regulate the blood pressure. Therefore, it is called long term
regulation.
Kidneys regulate arterial blood pressure by two ways:
1. Regulation of extracellular fluid volume (ECF)
2. Through renin angiotensin mechanism.

1. Regulation of extracellular fluid volume

When the blood pressure increases, kidneys excrete large amounts of water and salt, particularly sodium,
due to the mechanism called pressure diuresis and pressure natriuresis.
Pressure diuresis is the excretion of large quantity of water in urine because of increased blood
pressure. .Even a slight increase in blood pressure doubles the water excretion.
Pressure natriuresis is the excretion of large quantity of sodium in urine.
Because of water and Na urinary elimination decrease the ECF volume and blood volume, the arterial
blood pressure became normal.
When blood pressure decreases, the reabsorption of water from renal tubules is increased. This in turn,
increases ECF volume, blood volume and cardiac output, resulting in restoration of blood pressure.

2. Through renin-angiotensin mechanism

..
Actions of Angiotensin II
When blood pressure and ECF volume decrease, renin secretion from kidneys is increased. It converts
angiotensinogen which is synthetized in the liver into angiotensin I. This is converted into angiotensin II
in the presence of the ACE (angiotensin converting enzyme) at the pulmonary and renal level .
Angiotensin II acts to restore the blood pressure due to:
i. arterioles constriction so that the peripheral resistance is increased and blood pressure
rises. This include the afferent arterioles in kidneys constriction , so that glomerular
filtration is reduced. This results in retention of water and salts with the ECF volume
increasing. This in turn increases the blood pressure to normal level.
ii. Reabsorption of sodium and water due to it direct action at the tubular nephrons level or
due to the stimulation of the adrenal cortex to secrete aldosterone. This hormone
increases reabsorption of sodium from renal tubules. Sodium reabsorption is followed by
water reabsorption and ECF increasing.
iii. act at the pituitary gland level to release ADH or antidiuretic hormone which act on
collector ducks and increase the water reabsorption and ECF increasing
iv. increase the sympathetic activity with vasoconstriction

However, the amount of this hormone required to cause the vasopressor effect is very much high than
the amount required to cause the antidiuretic effect.

C.Hormonal mechanism for regulation of blood pressure

Many hormones are involved in the regulation of blood pressure . They can increase or decrease the
blood pressure .

a. Hormones which increase blood pressure

Hormones, which increase the arterial blood pressure have different mechanism of action.
1. Adrenaline
Adrenaline is secreted by the adrenal medulla. It is also released by sympathetic postganglionic nerve
endings. Adrenaline regulates the blood pressure by acting through heart and blood vessels. It increases
systolic pressure by increasing the force of contraction of the heart and cardiac output. It decreases
diastolic pressure by reducing the total peripheral resistance.
Adrenaline causes constriction of blood vessels through alpha receptors. It also causes dilatation of
blood vessels through β2receptors in some areas of the body like skeletal muscle, liver and heart. So,the
total peripheral resistance is reduced leading to decrease in diastolic pressure
2. Noradrenaline
Noradrenaline is secreted by the adrenal medulla. It is also released by sympathetic postganglionic nerve
endings. Noradrenaline increases diastolic pressure due to its general vasoconstrictor effect . It has
stronger effects on blood vessels than on the heart. It causes constriction of all blood vessels throughout
the body via alpha receptors. So it is called ‘general vasoconstrictor’. The action of noradrenaline is to
increase the total peripheral resistance and diastolic pressure. It also increases the systolic pressure
slightly, by increasing the force of contraction of heart.
3. Thyroxine
Thyroxine secreted form thyroid gland increases systolic pressure but decreases the diastolic pressure. It
increases the systolic pressure by increasing cardiac output. The cardiac output is increased because of
increase in the blood volume and force of contraction of the heart .Thyroxine has indirect action on
diastolic pressure.
Large quantities of metabolites are produced during increased metabolic activity induced by thyroxine.
These metabolites cause vasodilatation, leading to decrease in peripheral resistance. It causes decrease
in diastolic pressure. Generally, mean arterial pressure is not altered by the activity of thyroxine. Systolic
pressure is increased and the diastolic pressure is decreased. So, only the pulse pressure increases.
4. Aldosterone
Aldosterone is secreted from adrenal cortex. It causes retention of sodium and water and thereby,
increases the ECF fluid volume and blood volume, leading to increase in blood pressure. Thus, an
increase in the secretion of aldosterone increases the blood pressure by the increasing of the blood
volume.
5. Vasopressin or ADH (antidiuretic hormone)
Vasopressin or ADH, which is secreted by posterior pituitary has a potent action on the blood vessels,
particularly the arteries. It causes constriction of the arteries in all parts of the body. Due to the
vasoconstriction, the blood pressure is increased. However, the amount of this hormone required to
cause the vasopressor effectis very much high than the amount required to cause the antidiuretic effect
6. Angiotensins Angiotensin II, III and IV, which are obtained from angiotensinogen cause
constriction of systemic arterioles and elevate blood pressure.
7. Serotonin
Serotonin is otherwise known as 5-hydroxytryptamine. Serotonin is secreted from many sources it
increases the blood pressure by vasoconstriction.

b. Hormones which decrease blood pressure

Following hormones decrease the arterial blood pressure by causing vasodilatation:
1. Vasoactive Intestinal Polypeptide
Vasoactive intestinal polypeptide (VIP) is secreted in the stomach and small intestine. A small amount of
this hormone is also secreted in large intestine. VIP is a vasodilator and causes dilatation of peripheral
blood vessels and decrease in blood pressure.
2. Bradykinin
Bradykinin is produced in blood during the conditions like inflammation. During such conditions, the
enzyme in the blood called kallikrein is activated. It acts on α2globulin to form kallidin, which is converted
into bradykinin Bradykinin is a vasodilator substance and causes reduction in blood pressure.
3. Prostaglandins
Prostaglandin PGE2 is a vasodilator substance. It is secreted from almost all tissues of the body . It
decreases blood pressure.
4. Histamine
Histamine is secreted in nerve endings of hypothalamus, limbic cortex and other parts of cerebral cortex.
Histamine is also released from tissues during allergic conditions, inflammation or damage .Histamine
causes vasodilatation and decreases the blood pressure.
5. Acetylcholine
Acetylcholine is the cholinergic neurotransmitter released from many sources. Acetylcholine causes
vasodilatation and decreases the blood pressure.
6. Atrial Natriuretic Peptide
Atrial natriuretic peptide (ANP) is a hormone secreted by the atrial musculature of heart. It causes
dilatation of blood vessels and decreases the blood pressure .
7. Brain Natriuretic Peptide
Brain natriuretic peptide (BNP) is a hormone secreted by the atrial musculature of heart. Like ANP, this
hormone also causes dilatation of blood vessels and decreases the blood pressure.
8. C-type Natriuretic Peptide
C type natriuretic peptide (CNP) is secreted by several tissues including myocardium and vascular
endothelium . CNP decreases blood pressure by vasodilatation.

D. Local mechanism for regulation of blood pressure

In addition to nervous, renal and hormonal mechanisms, some local substances also regulate the blood
pressure.
The local substances regulate the blood pressure by vasoconstriction or vasodilatation.
1. Local vasoconstrictors
Local vasoconstrictor substances are derived from vascular endothelium. These substances are called
endothelium-derived constricting factors (EDCF).Common EDCF are endothelins (ET), which are
peptides with 21 amino acids. Three types of endothelins ET1,ET2 and ET3 are identified so far.
Endothelins are produced by stretching of blood vessels. These peptides act by activating phospholipase,
which in turn activates prostacyclin and thromboxane A2. These two substances cause constriction of
blood vessels and increase the blood pressure.
2. Local vasodilators
Local vasodilators are of two types:
1. Vasodilators of metabolic origin
2. Vasodilators of endothelial origin.
Vasodilators of Metabolic Origin
Vasodilators of metabolic origin are carbon dioxide, lactate, hydrogen ions and adenosine .
Vasodilators of Endothelial Origin
Nitric oxide (NO) is an endothelium derived relaxing factor (EDRF). It is synthesized from arginine. Nitric
oxide synthesis is stimulated by acetylcholine, bradykinin, VIP, substance P and platelet breakdown
products. As nitric oxide is a vasodilator, deficiency of this leads to constant vasoconstriction and
hypertension..

5. Blood pressure is measured by two methods:

A. Direct method
B. Indirect method.

6. Pathological variations of arterial blood pressure:

A. Hypertension
B. Hypotension.
A. Hypertension
Definition
Hypertension is defined as the persistent high blood pressure. Clinically, when the systolic pressure
remain elevated above 150 mm Hg and diastolic pressure remains elevated above 90 mm Hg, it is
considered as hypertension. If there is increase only in systolic pressure, it is called systolic
hypertension.

Types of Hypertension
Hypertension is divided into two types:
1. Primary hypertension or essential hypertension
2. Secondary hypertension.
1. Primary Hypertension or Essential Hypertension
Primary hypertension is the elevated blood pressure in the absence of any underlying disease. It is also
called essential hypertension. Arterial blood pressure is increased because of increased peripheral
resistance, which occurs due to some unknown cause.
2. Secondary Hypertension
Secondary hypertension is the high blood pressure due to some underlying disorders.
i. Cardiovascular hypertension
Cardiovascular hypertension is produced due to the cardiovascular disorders such as:
a. Atherosclerosis: Hardening of blood vessels due tofat deposition
b. Coarctation of aorta: Narrowing of aorta.
ii. Endocrine hypertension
of some endocrine glands:
a. Pheochromocytoma: Tumor in adrenal medulla, resulting in excess secretion of catecholamines
b. Hyperaldosteronism: Excess secretion of aldosterone from adrenal cortex
c. Cushing syndrome: Excess secretion of glucocorticoids from adrenal cortex.
iii. Renal hypertension
Renal diseases causing hypertension:
a. Stenosis of renal arteries
b. Tumor of juxtaglomerular cells, leading to excess production of angiotensin II
c. Glomerulonephritis.
iv. Neurogenic hypertension
Nervous disorders producing hypertension:
a. Increased intracranial pressure
b. Lesion in tractus solitarius
c. Sectioning of nerve fibers from carotid sinus.
v. Hypertension during pregnancy
Some pregnant women develop hypertension because of toxemia of pregnancy. Arterial blood pressure is
elevated by the low glomerular filtration rate and retention of sodium and water. It may be because It may
be because of some autoimmune processes during pregnancy or release of some vasoconstrictor agents
from placenta or due to the excessive secretion of hormones causing rise in blood pressure. Hypertension
is associated with convulsions in eclampsia.

B.Hypotension
Definition
Hypotension is the low blood pressure. When the systolic pressure is less than 90 mm Hg, it is
considered as hypotension.
Types
1. Primary hypotension
2. Secondary hypotension.
1. Primary hypotension
Primary hypotension is the low blood pressure that develops in the absence of any underlying disease
and develops due to some unknown cause. It is also called essential hypotension. Frequent fatigue and
weaknessare the common symptoms of this condition. However, the persons with primary hypotension
are not easily
susceptible to heart or renal disorders.
2. Secondary hypotension
Secondary hypotension is the hypotension that occurs due to some underlying diseases. Diseases, which
cause hypotension are:
i. Myocardial infarction
ii. Hypoactivity of pituitary gland
iii. Hypoactivity of adrenal glands

Orthostatic hypotension
Orthostatic hypotension is the sudden fall in blood pressure while standing for some time. It is due to the
effect of gravity. It develops in persons affected by myasthenia gravis or some nervous disorders like
tabes dorsalis, syringomyelia and diabetic neuropathy. Common symptom of this condition is orthostatic
syncope.

Capillary pressure

Definition
Capillary pressure is the pressure exerted by the blood contained in capillary. It is also called capillary
hydrostatic pressure.
Capillary hydrostatic pressure (Pc) depends on arteriolar and venular pressures as well as on the relation
of the precapillary to the postcapillary resistance .

Significance
Capillary pressure is responsible for the exchange of various substances between blood and interstitial
fluid through capillary wall.
The walls of the capillaries are thin and constructed of single-layer, highly permeable endothelial cells.
Therefore, water, cell nutrients, and cell excreta can all interchange quickly and easily between the
tissues and the circulating blood.
The peripheral circulation of the entire body has about 10 billion capillaries with a total surface area
estimated to be 500 to 700 square meters (about one eighth the surface area of a football field). Indeed, it
is rare that any single functional cell of the body is more than 20 to 30 micrometers away from a capillary.
Normal Values
Blood usually does not flow continuously through the capillaries. Instead, it flows intermittently, turning on
and off every few seconds or minutes. The cause of this intermittency is the phenomenon called
vasomotion, which means intermittent contraction of the met arterioles and precapillary sphincters (and
sometimes even the very small arterioles).
Generally, the pressure in the arterial end of the capillary is about 30 to 32 mm Hg and in venous end it is
15 mmHg. However, capillary pressure varies depending upon the function of the organ or region of the
body.
„ REGIONAL VARIATIONS
Regional variation in capillary pressure is in relation to the physiological activities of the particular region.
So,it has some functional significance. Capillary pressure remarkably varies in kidneys and lungs.

Capillary Pressure in Kidneys

In kidneys, the glomerular capillary pressure is high. It is about 60 mm Hg. This high capillary pressure is
responsible for glomerular filtration.
Capillary Pressure in Lungs
In lungs, the pulmonary capillary pressure is low and it is about 7 mm Hg. It favors exchange of gases
between blood and alveoli.

„ MEASUREMENT
(1) direct micropipette cannulation of the capillaries, which has given an average mean capillary pressure
of about 25 mm Hg in some tissues such as the skeletal muscle and the gut,
(2) indirect functional measurement of the capillary pressure, which has given a capillary pressure
averaging about 17 mm Hg in these tissues.
Direct Method
Capillary pressure was first measured by EM Landis, when he was a medical student. Minute vessels in
the web of foot in a frog were cannulated by using micropipette, with a diameter of 5 μ at the tip with the
aid of microscope.
The cannula was connected to a manometer. This method was later followed to measure capillary
pressure in other organs.
Indirect Method
Indirect method is based upon the principle of exerting an external pressure necessary to obstruct the
flow of blood in capillaries. The capillaries are observed under microscope.

REGULATION

Arterioles play an important role in regulating the capillary pressure and the pressure in capillaries is
considered as a function of arteriolar resistance.
When the arterioles constrict, resistance increases in arterioles, which raises the arterial blood pressure.
At the same time, the volume of blood flowing into capillaries decreases, leading to fall in capillary
pressure.
On the other hand, during dilatation of arterioles, the resistance decreases and arterial blood pressure
decreases. But the capillary pressure increases because of increase in volume of blood flowing into
capillaries
According to Poiseuille’s law, the resistance (Ri) of an individual, unbranched vascular segment is
inversely proportional to the fourth power of the radius Thus, the pressure drop between any two points
along the circuit depends critically on the diameter of the vessels between these two points. However, the
steepest pressure drop (ΔP/Δx) does not occur along the capillaries, where vessel diameters are
smallest, but rather along the precapillary arterioles. Why? The aggregate resistance contributed by
vessels of a particular order of arborization depends not only on their average radius but also on the
number of vessels in parallel. The more vessels in parallel, the smaller the aggregate resistance .
Although the resistance of a single capillary exceeds that of a
single arteriole, capillaries far outnumber arterioles . The result is that the aggregate resistance is larger in
the arterioles, and this is where the steepest ΔP occurs.
The most important factor affecting the degree of opening and closing of the metarterioles and
precapillary sphincters that has been found thus far is the concentration of oxygen in the tissues. When
the rate of oxygen usage by the tissue is great so that tissue oxygen concentration decreases below
normal, the intermittent periods of capillary blood flow occur more often, and the duration of each period
of flow lasts longer, thereby allowing the capillary blood to carry increased quantities of oxygen (as well as
other nutrients) to the tissues.
CAPILLARY ONCOTIC PRESSURE
the four primary forces that determine whether fluid will move out of the blood into the
interstitial fluid or in the opposite direction. These forces, called “Starling forces” in honor of the
physiologist Ernest Starling, who first demonstrated their importance, are:
1. The capillary pressure (Pc), which tends to force fluid outward through the capillary membrane.
2. The interstitial fluid pressure (Pif), which tends to force fluid inward through the capillary membrane
when Pif is positive but outward when Pif is negative.
3. The capillary plasma colloid osmotic pressure (Πp), which tends to cause osmosis of fluid inward
through the capillary membrane.
4. The interstitial fluid colloid osmotic pressure (Πif), which tends to cause osmosis of fluid outward
through the capillary membrane.

Capillary membrane is permeable to all substances except plasma proteins. So, the plasma proteins stay
within the capillaries and exert some pressure which is called oncotic pressure or colloidal osmotic
pressure.
Normal oncotic pressure is about 25 mm Hg. Among the plasma proteins, albumin exerts 70% of oncotic
pressure.
Oncotic pressure plays an important role in filtration across capillary membrane, particularly in renal
glomerular capillaries.
If the sum of these forces—the net filtration pressure— is positive, there will be a net fluid filtration across
the capillaries. If the sum of the Starling forces is negative, there will be a net fluid absorption from the
interstitial spaces into the capillaries. The net filtration pressure (NFP) is calculated as NFP = Pc − Pif −p
−if