ARTERIAL BLOOD PRESSURE

AND ITS REGULATION

AGE AND SEX VARIATIONS IN BLOOD
PRESSURE
• Normal arterial blood pressure varies with age and sex.
Between the ages of 20 and 30 years systolic and
diastolic blood pressures are lower in women than in
men.
• In a healthy young person systolic pressure is 110 –
120mmHg and diastolic is 70 – 80mmHg.
• As a person ages both systolic and diastolic pressures
increase but there is usually a greater increase in the
systolic.
The mean arterial pressure (MAP) is the mean pressure head
that propels blood to the tissues ensuring tissue perfusion.
It is not just an average of systolic and diastolic pressure because
diastole lasts longer than systole; therefore MAP is closer to
diastolic than to the systolic pressure.
MAP is obtained by adding a third of the pulse pressure to the
diastolic pressure.
The pulse pressure is the difference between systolic and
diastolic pressure. In a subject with a blood pressure of
120/70mmHg:
Pulse pressure = 120 – 70mmHg = 50mmHg
MAP = 70 + 50/3 = 86mmHg
REGULATION OF BLOOD PRESSURE
The regulation of blood pressure is a classic example of homeostatic
regulation.
 It depends on the regulation of two variables namely:
 peripheral resistance and cardiac output.
Blood pressure = Cardiac Output × peripheral resistance
The peripheral resistance is very much dependent on the diameter of the
blood vessels.
The neural center that controls changes in the diameter of the blood vessels
is the vasomotor center (VMC) made up of a cluster of cells in the medulla.
 The vasomotor center and the cardiac center are collectively called the
cardiovascular center.
The cardiovascular center integrates blood pressure control by altering
cardiac output and blood vessel diameter.
THE VMC
The VMC sends impulses at a fairly steady rate along sympathetic
efferents called vasomotor fibers which exit from the T1 through L2
levels of the spinal cord to innervate smooth muscles of the blood
vessels especially the arterioles. As a result the arterioles are almost
always in a state of moderate constriction called vasomotor tone
The degree of vasomotor tone varies from organ to organ. For
example vessels of the skin and digestive system receive vasomotor
impulses more frequently and so tend to be more constricted than
vessels in the skeletal muscles.
Increase in sympathetic activity causes generalized vasoconstriction
and increase in blood pressure while decreased sympathetic activity
allows vascular muscles to relax and lowers blood pressure.
MECHANISMS FOR BLOOD PRESSURE
REGULATION
The day to day maintenance of arterial blood pressure
depends on the baroreceptor reflex, but long term
regulation depends on intrinsic renal mechanisms. In
emergencies such as haemorrhage with shock these
mechanisms are supplemented by other mechanisms such as:
Other neural reflexes e.g. chemoreceptor and CNS
ischaemic reflexes
Fluid shifts from interstitial space to blood capillaries
Hormonal mechanisms e.g. Renin – Angiotensin –
aldosterone mechanism, ADH and atrial natriuretic
hormone mechanism.
SHORT - TERM NEURAL REFLEXES
FOR BLOOD PRESSURE REGULATION
BARORECEPTOR REFLEX
CHEMORECEPTOR REFLEX
CNS ISCHAEMIC REFLEX
THE BARORECEPTOR REFLEX
Baroreceptors are stretch receptors in the walls of the heart and
the blood vessels which are stimulated when there is a rise in
arterial blood pressure. They are found in the high and low
pressure sections of the circulation.
The baroreceptors in the high pressure section are found in the
carotid sinuses, aortic arch and most of the large vessels of neck
and thorax.
The baroreceptors for the low pressure section are located in
the atria, the great veins and the pulmonary artery. They are
essentially volume receptors and since increase in blood volume
results in raised blood pressure they indirectly monitor arterial
blood pressure.
When stimulated afferents from the aortic sinus and
carotid sinus run in the vagus and glossopharyngeal
nerves respectively and terminate in the nucleus tractus
solitarius. From the nucleus tractus solitarius facilitatory
connection is made with the nucleus ambiguous of the
vagus and through interneurons inhibitory connections
are made to neurons of the VMC.
The threshold for the excitation of the high pressure
baroreceptors is at least 60mmHg and their functional
range is 60 – 180mmHg. This means that in the normal
range of arterial blood pressure these receptors are
tonically active thus exerting a tonic inhibition of the
VMC while facilitating the vagus.
Baroreceptors respond both to rate of rise in arterial
blood pressure (dynamic response) and the degree of
rise (static response). Rapid changes in arterial
pressure are more effective in stimulating
baroreceptors than slow changes.
THE MECHANISM
 A rise in blood pressure causes a prompt increase in impulses
along the baroreceptor afferents which inhibit the VMC.
Inhibition of VMC results in peripheral vasodilation and
slowing of the heart causing a fall in peripheral resistance and
cardiac output and therefore a lowering of the blood pressure.
Conversely a fall in blood pressure e.g. as occurs in
hypovolemic shock reduces stretch on the baroreceptors and
the impulses along their afferents diminish. This removes
baroreceptor inhibition of the VMC and withdraws the
facilitation of the vagus. This allows the tonic sympathetic
discharge of the VMC free course resulting in widespread
vasoconstriction, tachycardia and an increase in stroke volume.
The outcome is an increase in peripheral resistance, cardiac
output and ultimately a rise in blood pressure to the normal
level.
ADAPTATION
 Baroreceptors adapt after 2 – 3 days of responding to
new blood pressures no matter the level of the
pressure.
 After the initial brisk response to a rise in pressure the
frequency of impulses in the baroreceptor afferents
drops rapidly at first, then more slowly till it returns to
its resting firing rate .
 This behavior makes baroreceptor reflexes unsuitable
for long term regulation of blood pressure.
THE CHEMORECEPTOR REFLEX
A fall in blood pressure below 60mmHg
(baroreceptors are not active at this level) slows blood
flow to tissues causing hypoxia, hypercapnia and
acidosis.
 These chemical changes stimulate chemoreceptors in
the carotid bodies and medulla causing an increase in
respiration and stimulation of the VMC to raise the
blood pressure and increase blood flow to the tissues.
This reflex becomes active in emergencies like massive
haemorrhage but their role is limited because of the
direct effect of hypoxia, hypercapnia and acidosis to
cause vasodilation which antagonizes the reflex effect.
CNS ISCHAEMIC RESPONSE
When the blood pressure drops to dangerously low
levels e.g. 50mmHg and below, there is inadequate
blood flow to neurons of VMC; the resultant hypoxia
stimulates the VMC neurons directly and strongly.
The effect is a powerful sympathetic discharge causing
vasoconstriction on a scale not seen in any other
condition, which is capable of raising the systolic
blood pressure to 270mmHg for a period of about 10
minutes.
This response is maximal at arterial pressures of about
15mmHg and is thus considered a ‘last ditch stand’
after which, if ischaemia of the VMC persists the
neurons begin to die.
A special case of CNS ischaemic response is called the
Cushing reaction.
 Raised intracranial pressure (e.g. due to space
occupying lesion) compresses the arteries of the brain
and activates the CNS ischaemic response raising
arterial blood pressure above the compression
pressure so that blood continues to flow into the brain.
SHORT – TERM HORMONAL
MECHANISMS FOR BLOOD
PRESSURE REGULATION
CATECHOLAMINES
RENIN – ANGIOTENSIN MECHANISM
ATRIAL NATRIURETIC PEPTIDE
A fall in blood pressure causes release of
catecholamines, Angiotensin II and vasopressin
(ADH). Being hormones their actions are slower to
respond to changes in blood pressure than the neural
reflexes described earlier.
CATECHOLAMINES
Sympathetic discharge from the VMC causes the adrenal
medulla to release adrenaline and noradrenaline which
circulates in blood increasing cardiac output and
vasoconstriction and so supplements the action of the
sympathetic nervous reflexes.
 During periods of stress these hormones are released from
the adrenal gland and they enhance the sympathetic fight –
flight response.
NB. That nicotine causes intense generalized vasoconstriction
both by direct sympathetic stimulation and also by increasing
release of large amounts of adrenaline and noradrenaline.
RENIN – ANGIOTENSIN MECHANISM
When blood pressure or blood volume is low the kidneys are
caused to release the hormone renin. Renin acts as an enzyme
that ultimately generates Angiotensin II which:
Promotes intense vasoconstriction resulting in a rapid rise in
systemic blood pressure.
Stimulates increased renal sodium and water reabsorption
directly and through the release of aldosterone from adrenal
cortex. Aldosterone acts in long term blood pressure regulation
to increase renal sodium and water reabsorption
Stimulates the hypothalamus to provoke thirst and to release
ADH which cause increased water reabsorption in the renal
tubules.
ATRIAL NATRIURETIC PEPTIDE (ANP)
 Increase in blood pressure or blood volume stretches
atrial musculature causing it to secrete this
polypeptide hormone ANP.
 ANP antagonizes aldosterone and causes the kidney
to excrete more sodium and water from the body
resulting in a decrease in blood volume.
 It also causes generalized vasodilation.
MEDIUM – TERM MECHANISM
FLUID REABSORPTION FROM INTERSTITIAL
SPACE
A fall in blood pressure promotes fluid reabsorption
from interstitial space into the blood capillaries. After a
moderately severe haemorrhage the shift starts within
minutes and is well established within an hour. Up to
250 ml could shift into the blood circulation within 24
hours. This helps to restore circulating blood volume,
raise the blood pressure and relieve the vasoconstriction
caused by the sympathetic reflexes.
LONG TERM MECHANISM
RENAL REGULATION
The kidneys help maintain blood pressure homeostasis
by regulating blood volume. They act both directly and
indirectly to regulate arterial blood pressure and so
provide the major long term mechanism for blood
pressure control.
THE DIRECT RENAL MECHANISM
alters blood volume independently of hormones.
When blood volume or blood pressure rises, the speed
at which fluid filters from the blood stream into the
renal tubules increase. The kidneys are not able to
process the filtrate rapidly enough so more of it leaves
the body as urine.
As a result blood volume and blood pressure falls.
When blood volume or pressure is low the kidneys
conserve water and electrolytes, return them to the
blood stream and blood volume and pressure rises.
THE INDIRECT RENAL MECHANISM
the Renin – Angiotensin - Aldosterone Mechanism. When
arterial blood pressure declines the kidneys release the
enzymatic hormone renin into blood. Renin triggers a series
of reactions that produce Angiotensin II which increases
blood pressure in 3 main ways:
As a potent vasoconstrictor , increasing peripheral resistance
By stimulating adrenal cortex secretion of aldosterone , a
hormone that enhances renal absorption of sodium and
consequently water.
It causes the posterior pituitary to release ADH which further
promotes water reabsorption.
It also triggers the thirst sensation leading to increased water
consumption. Ultimately resulting in a raise in blood volume
and blood pressure.
HYPERTENSION
There is wide individual variation in normal blood pressure
but blood pressure that remains persistently above
160/90mmHg is associated with increased risk of stroke.
Hypertension is more severe and common in blacks than in
whites and is made worse by obesity, smoking and heavy
alcohol consumption (risk factors).
The hypertension may be mainly systolic or diastolic and
may occur in systemic arteries (systemic hypertension) or
less commonly in pulmonary arteries (pulmonary
hypertension).
A sustained rise in blood pressure implies that there is an
abnormal increase in either cardiac output or peripheral
resistance beyond the capacity of the regulatory
mechanisms.
CAUSES OF HYPERTENSION

These can be remembered with the acronym RECTI

R – RENAL
E – ENDOCRINE
C – COARCTATION OF THE AORTA
T – TOXAEMIA OF PREGNANCY
I – IDIOPATHIC
IDIOPATHIC (ESSENTIAL HYPERTENSION):
In about 90% of cases cause of hypertension is not
known therefore is referred to as idiopathic or
essential hypertension. In about 70% of these
individuals there is a family history of hypertension
suggesting a strong hereditary role. In all case the
dominant feature is an increase in peripheral
resistance.
RENAL HYPERTENSION
 Kidney disease can cause hypertension through the
rennin – Angiotensin mechanism or through salt and
water retention. In chronic renal disease ischaemic
areas secrete rennin and salt and water retention
occurs in both ischaemic areas and normal areas.
ENDOCRINE OR HORMONAL CAUSES
Hypertension may be due to endocrine disorders such
as Conn’s syndrome ( primary hyperaldosteronism),
phaeochromocytoma (excess catecholamines from
adrenal medulla tumor), Cushing’s syndrome (excess
glucocorticoids) and acromegaly (excess growth
hormone). Some women on contraceptives may
develop hypertension b/c estrogens stimulate
production of angiotensinogen.
COARCTATION OF AORTA
 In this congenital anomaly the aorta is constricted at a
point beyond the origin of the carotids and left
subclavian arteries. Resistance to flow through the
aorta causes hypertension in upper parts of the body
but near vnormal pressure in lower parts.
TOXAEMIA OF PREGNANCY
Is a complication of pregnancy characterized by
edema, proteinuria and hypertension. The
hypertension is believed to be caused by polypeptide
vasoconstrictors secreted by the placenta.