MEDIUM TO LONG-TERM

REGULATION OF BLOOD PRESSURE

Prof Lam Sau Kuen
Department of Physiology

2014.11.19 Wed

MBBS Stage II UMMP Class of 2013

Blood Pressure

Pull out, Betty! Pull out! . . . Youve hit an artery!

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Learning Objectives
Normal arterial blood pressure (BP)
Regulation of BP
Short-term regulation of BP
Baroreceptor reflex
Chemoreceptor reflex
Central nervous system (CNS) ischaemic response
Medium to long-term regulation of BP
Renin-angiotensin-aldosterone system (RAAS)
Role of the kidney in long-term regulation
High BP (hypertension)
Guidelines
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NORMAL ARTERIAL BP

Pressure on Vessel Walls

BP is the lateral pressure
exerted by a volume of blood
on the walls of the blood
vessels as it flows through the
vessels

Arterial BP BP in aorta and

arteries
Venous BP BP in veins

Arterial Blood Pressure

Systolic and diastolic BP
Systolic BP (SBP):
120 mmHg (90 130 mmHg)
Highest pressure recorded when
left ventricle is contracting
(systole)
Exerting maximal force on blood
Diastolic BP (DBP):
80 mmHg (60 90 mmHg)
Lowest pressure recorded when
left ventricle is relaxing (diastole)
Due to elastic recoil and arteriolar
resistance
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Arterial BP
Normal BP: 120/80 mmHg
Pulse pressure (PP)
PP = SBP DBP
PP = 120 80 = 40 mmHg
Mean arterial pressure (MAP)
MAP = DBP + 1/3 PP
MAP = 80 + 13.3 = 93.3
mmHg (~100 mmHg)
Mean pressure in arteries
during a cardiac cycle
Mean driving force to push
blood through capillaries
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Importance of normal MAP

To ensure adequate driving force to perfuse tissue
To prevent extra heavy load on heart (afterload)
To prevent damage to blood vessels

Arterial (Systemic) and Pulmonary BP

Determinants of BP

BP is dependent upon:
Cardiac output (CO)
Total peripheral resistance (TPR)
Blood volume

BP is given by:
BP = CO x TPR
CO = SV X HR

BP = SV X HR X TPR

Changes in SV or HR or TPR or blood volume will alter BP

Each of these factors can be manipulated by drug therapy

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Factors Affecting Cardiac Output

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TPR
TPR or systemic vascular resistance (SVR):
Amount of friction against blood flow
Determined by
Sympathetic activity
Diameter of arterioles (resistance vessels)

TPR
(vasodilation)

TPR
(vasoconstriction)
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Summary of Factors affecting BP

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REGULATION OF BP

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Regulation of BP

Short-term regulation
Fast
Sec-to-sec
Spurts
Neural (autonomic reflexes)
Baroreceptor mechanism
Acts by changing CO or TPR
For survival

Medium to long-term regulation

Slow
Min-to-min, hour-to-hour, day-to-day, month-to-month, year-to-year
Basal level
Hormonal
Renin-angiotensin-aldosterone system (RAAS)
Involves the kidneys
Acts by regulating blood volume through kidneys
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Short-term Regulation of BP
Responds within seconds to
daily ambulatory changes in
BP
Involves autonomic reflexes
Baroreceptor mechanism
(reflex) (main)
Chemoreceptor reflex
CNS ischaemic response
Regulates BP by altering CO
or TPR
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Baroreceptor Mechanism

Afferent nerves:
Vagus
Glossopharyngeal

Integrating centre:
Cardiovascular
centre (CVC) in
medulla

Sensory organs:
Baroreceptors in
carotid sinus +
aortic arch
Negative feedback
Stimulus: or in BP

Efferent nerves:
Sympathetic
Parasympathetic

Effector organs:
Heart
- SA node
- Ventricle
Arterioles
Response: or in BP17

Sensory Organs: Baroreceptors

Stretch receptors
Respond to blood pressure changes
Located in carotid sinus and aortic arch
Also in large arteries of neck and thorax

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Integrating Centre: Cardiovascular

Centre (CVC) in Medulla

CVC

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Effector Organs: Heart and Arterioles

Sympathetic stimulation:
rate of SA node and conduction
velocity in the AV node
force of contraction of
myocardium
Vaso- and venoconstriction
Parasympathetic stimulation:
excitability of both SA and AV
node by hyperpolarizing the
membrane during diastole

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Baroreceptor Reflex

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Baroreceptor Reflex: When BP increases

BP:

stretch of baroreceptors
impulses generated
impulses to CVC
CVC inhibited
sympathetic outflow
parasympathetic outflow

to heart:
to arterioles:

HR, force of contraction, SV

CO
vasodilation
TPR

BP = SV X HR X TPR
BP

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Baroreceptor Reflex: Increase in BP

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Baroreceptor Reflex: When BP decreases

BP:

stretch of baroreceptors
impulses generated
impulses to CVC
CVC not inhibited
sympathetic outflow
parasympathetic outflow
to heart:

HR, force of contraction, SV

CO
to arterioles: vasoconstriction
TPR
BP = SV X HR X TPR
BP
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Baroreceptor Reflex: Decrease in BP

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Chemoreceptor Reflex
Chemoreceptors
Carotid bodies
Aortic bodies
Respond to:
Increase in plasma CO2 (decrease in
pH)
More sensitive
Decrease in O2
Less sensitive
Impulse sent to CVC
Increase sympathetic outflow
Increase HR and force of contraction
Increase in CO and hence BP
More blood flows to lungs for removal
of CO2 and intake of O2
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CNS Ischaemic Response

Last ditch response to increase BP

Stimulus: MAP < 60 mmHg

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Long-term Regulation of BP
Medium to long-term regulation
Slow
Min-to-min, hour-to-hour, day-today, month-to-month, year-toyear
Involves hormonal regulation of
blood volume by kidneys
By controlling water balance
Water intake = water
output
Antidiuretic hormone
(ADH) or arginine
vasopressin (AVP)
By controlling Na+ balance
Na+ intake = Na+ output
RAAS
Natriuretic peptides (NP)
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Water Balance

AVP
Hormone that regulates ECF fluid
volume
Synthesised in hypothalamus
Stored and released from posterior
pituitary gland
Triggers for secretion
Hypovolaemia
Hypotension
Extracellular hyperosmolarity
Angiotensin II
Sympathetic stimulation
Acts on renal collecting ducts via V2
receptors to increase reabsorption of
water
Increases blood volume, CO and hence
BP
Also causes vasoconstriction
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Water Balance
Water intake = water output

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Na+ Balance

Na+ intake = Na+ output

Na+
Most important ECF ion
Most abundant ion
Major determinant of ECF vol
Thus determines BP

Controlled by RAAS
Reabsorption of Na+

Counter-regulated by natriuretice peptides (NP)

Atrial NP (ANP) from atrial walls
Brain BP (BNP) from ventricular walls
Excretion of Na+

Handled by kidneys
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Renal Regulation of Blood Pressure

In the kidney
Juxtaglomerular apparatus (JGA)

Located in cortex

Unique segment:
Thick ascending limb of the loop of
Henle passes between the afferent
and efferent arterioles of its own
glomerulus

Three special tissues:

Macula densa point of contact
between ascending limb and
arterioles (modified thick aLoH cells)
JG cells modified smooth muscle
cells of afferent arterioles (granular
cells) that synthesise and secrete
renin
Lacis cells (extraglomerular
mesangial cells), not granular but also
secrete renin
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JGA

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Sensory Receptors in JGA

Two sensors are present in the JGA
In macula densa
Sensory receptors that detect changes
in Na+ concentration in tubular fluid of
PCT
In afferent arteriole
Baroreceptors (stretch receptors) that
detect changes in perfusion pressure
of arterial blood
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Renal Regulation of Blood Pressure

Decrease in BP perfusion pressure
Or Na+ filtered concentration in tubular
fluid
Results in stimulation of renin secretion from
JG cells
Renin angiotensin II formation
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Renal Regulation of Blood Pressure

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Renal Regulation of Blood Pressure

Role of kidneys

Aldosterone increased Na+ (and

water) reabsorption from CD
Action of ADH on vasopressin
receptors (V2) increased water
reabsorption from CD
Result in ECF volume expansion and an
increase in BP
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Renal Regulation of Blood Pressure

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Maintenance of Blood Pressure Homeostasis

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Figure 26.9

HYPERTENSION

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Hypertension

Guidelines
WHO-ISH: 140/90 mmHg (MAP 106.7, normal 93.3,
set-point resets)
JNC-VII:
140/90
Optimum <120/<80 (115/75 new normal)
>120/>80 now considered to be pre-hypertension
higher risk of developing hypertension
BHS:
140/90
Malaysia: 140/90

Risk is important and in diabetes: 130/80 mmHg

Two types:
Primary cause largely unknown etiology poorly
understood
Secondary cause known due to disease process
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High Blood Pressure: Risk Factors

Age
Race
Heredity (Bad genes)
Diet high fat and salt
Stress
Inactivity
Obesity
Smoking
Alcohol consumption
Diabetes
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High Blood Pressure: Symptoms

Silent killer
Patients are usually asymptomatic until
substantial vascular damage occurs
In more severe cases
Persistent throbbing headaches
Blurred vision
Nausea and vomiting
Ringing in ears - tinnitus
Chest pain
Swollen feet
Mini-strokes

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Treating
Hypertension

Lifestyle
Changes

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Treating Hypertension
CLASSES OF DRUGS

MECHANISM OF ACTION

Diuretics

Increase urine volume

Beta-blockers

Decrease HR
Decrease ventricular contractility

Calcium antagonists/blockers

Block Ca2+ channels

Vasodilation

ACE inhibitors

Inhibit conversion of angiotensin I to

angiotensin II
Vasodilation

Angiotension II-receptor
antagonists

Block receptors
Vasodilation

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