Md.

Jabiur Rahaman
Daffodil International University
Dept. Of pharmacy

Topic:Control of Blood
pressure
 Control of blood pressure
 Mean blood pressure is controlled by changing
total peripheral resistance and or cardiac output.

 Cardiac output is controlled by sympathetic and para

sympathetic nerves which effect:
 heart rate
 force of contraction

 TPR controlled by nervous and chemical means to effect

constriction/dilatation of
 arterioles and venules
Regulation of blood pressure
How is pressure “measured”?

 Short term
 Baroreceptors
 Long term
 Kidney via renin angiotensin system
Location of
baroreceptors

• Baroreceptors sense stretch and

rate of stretch by generating
action potentials (voltage spikes)

• Located in highly distensible

regions of the circulation to
maximise sensitivity
Baroreceptor output
(from single fibres)

Rapid increase in mean pressure Rapid decrease in mean pressure

Response to pulse pressure

From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)
 Two types of baroreceptor

 Type A
 High sensitivity
 High firing rate
 Type C
 Lower sensitivity
 Lower firing rate
 Higher threshold (before firing starts)
 Therefore can deal with higher pressures than type A which
become “saturated”

From “An Introduction to Cardiovascular Physiology”

J.R. Levick
 Baroreceptor reflex
Blood pressure falls

Sensors Aortic arch Carotid sinus

Neural integration Nucleus tractus solitarius

Vasoconstriction Cardiac stimulation Cardiac inhibition

Effectors Constriction of veins Increased stroke Increased heart

& arterioles volume rate

Increased peripheral Increased cardiac

resistance output

Increased blood
pressure
 Other stretch receptors

 Coronary artery baroreceptors

 Respond to arterial pressure but more sensitive than
carotid and aortic ones

 Veno-atrial mechanoreceptors
 Respond to changes in central blood volume
 Lie down, lift your legs and cause peripheral vasodilatation

 Unmyelinated mechanoreceptors
 Respond to distension of heart
 Ventricular ones during systole; atrial ones during inspiration
 Other receptors
 Heart chemosensors
 Cause pain in response to ischaemia
 K+, lactic acid, bradykinin, prostaglandins
 Arterial chemosensors
 Stimulated in response to
 Hypoxaemia, hypercapnia*, acidosis, hyperkalaemia**
 Regulate breathing
 Lung stretch receptors
 Cause tachycardia during inspiration

*too much CO2

**too much K+
Overview of short-term control mechanisms

From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)
Long term control of blood pressure
 Involves control of blood volume/sodium balance
by the kidneys
 Hormonal control
 Renin-angiotensin-aldosterone system
 Antidiuretic hormone (vasopressin)
 Atrial natiuretic peptide
 Pressure natriuresis
 Renin/angiotensin/
Reduced renal
blood flow aldosterone system
Increased
Juxtaglomerular blood volume
apparatus LV filling pressure)

Increased
Renin Fluid re-absorption pre-load

(LV pressure
Angiotensinogen Sodium retention
beginning of systole)

Increased
after-load
Angiotensin I
Increased aldosterone
Angiotensin II secretion

Veins
vasoconstriction
Arteries
Atrial natiuretic peptide

 Increases salt excretion via kidneys

 By reducing water reabsorption in the
collecting ducts
 relaxes renal arterioles
 inhibits sodium reabsorption in the distal
tubule

 Released in response to stimulation of atrial

receptors
Effect of blood loss
 less than 10%, no serious symptoms
 e.g. blood transfusion
 20 - 30% blood loss not usually life threatening
 greater than 30%, severe drop in BP and, often,
death due to impaired cerebral and coronary
perfusion