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
