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Topic:Control of Blood
pressure
Md.Jabiur Rahaman
Daffodil International University
Dept. Of pharmacy
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 decrease in mean pressure
From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)
Rapid increase in mean pressure
Response to pulse pressure
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
Aortic arch Carotid sinus
Constriction of veins
& arterioles
Increased stroke
volume
Increased heart
rate
Vasoconstriction Cardiac stimulation Cardiac inhibition
Nucleus tractus solitarius
Increased peripheral
resistance
Increased cardiac
output
Increased blood
pressure
Neural integration
Sensors
Effectors
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
Arteries
Veins
Reduced renal
blood flow
Juxtaglomerular
apparatus
Renin
Angiotensinogen
Angiotensin I
Angiotensin II
Increased
pre-load
Increased
after-load
vasoconstriction
Increased aldosterone
secretion
Sodium retention
Fluid re-absorption
Increased
blood volume
Renin/angiotensin/ aldosterone system
LV filling pressure)
(LV pressure
beginning of systole)
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