Blood pressure regulation and
tissue blood flow
Reverend Dr David CM Taylor
http:/www.liv.ac.uk/~dcmt
Learning outcomes
 Define the term blood pressure – systolic, diastolic,
mean arterial pressure
 Regulation of blood pressure (receptors and
hormones)
 Fluids and fluid volumes
 Renin angiotensin system – what triggers renin
 Concept of negative feedback loop
Blood Pressure
 Depends upon the amount of blood leaving the heart
 cardiac output
 and the resistance of the vasculature
 total peripheral resistance
Peripheral Resistance
Which will give the greater flow ?
Peripheral resistance 2
Which will give the greater flow ?
Cardiac Output
 Heart rate x stroke volume
End diastolic volume - End systolic volume
Stroke volume
Cardiac output
Heart rate
Putting this together
Stroke volume
Cardiac output
Heart rate
Cardiac output x Total peripheral resistance
Blood pressure
Chapter 18, p 207 in Preston and Wilson (2013)
Chapter 11, p 525 in Naish and Court (2014)
Pressures
 Systolic pressure is the result of contraction (systole)
 Diastolic pressure is when the heart is relaxed (diastole)
 Pulse pressure is the difference between them
 Mean arterial pressure is estimated as
 Diastolic pressure + 1/3(pulse pressure)
 This is because the pulse is not a sine wave
 Strictly speaking we should include central venous pressure
(but it is usually small enough to be ignored)
Chapter 19, p 219 in Preston and Wilson (2013)
Chapter 11, p 554 in Naish and Court (2014)
Fluids
 In a male 60% of body weight is due to fluid, in a
female 55%
 2/3 of the fluid is inside cells – intracellular fluid (ICF)
 1/3 is extracellular (ECF)
 Of the ECF 80% is interstitial fluid
 And 20% is plasma
 Osmotic pressure and hydrostatic pressure determine
the flow between interstitial fluid and plasma
Chapter 3, p 30 in Preston and Wilson (2013)
Chapter 2, p 20 in Naish and Court (2014)
Postulated mechanism for
hypertension
 Increased sympathetic activity
 Leads to increased cardiac output
 And peripheral vasoconstriction (to protect the capillary
beds)
 Drop in blood flow
 Triggers renin-angiotensin system
Evidence
 Cross transplantation studies show that essential
hypertension has its origins in the kidneys.
 Human and animal studies
 So does renal denervation
 Little evidence that “stress” is involved in essential
hypertension
 But, of course, drugs that decrease sympathetic activity
lower blood pressure.
Beevers, G., Lip, G. Y. H., & O’Brien, E.
(2001). The pathophysiology of
hypertension. BMJ : British Medical Journal,
322 (7291), 912–916.
Control
Autonomic N.S.
Volume
ADH
Pressure
Chemicals
Local Blood
Flow
Angiotensin
Pressure
 Sensed by baroreceptors
 in carotid arteries and aortic arch
 an increase in pressure causes a decrease in
sympathetic activity
 a decrease in pressure causes an increase in
sympathetic activity
Chapter 20, p 236 in Preston and Wilson (2013)
Chapter 11, p 554 in Naish and Court (2014)
Volume
 Sensed by atrial volume receptors
A decrease in volume
 causes an increase in ADH secretion
 and a decrease in ANF secretion
Chapter 20, p 244 in Preston and Wilson (2013)
Chapter 11, p 556 in Naish and Court (2014)
Chemicals
A decrease in O2, or more usually an increase in CO2 or
H2 causes an increase in chemoreceptor activity which
 increases sympathetic activity
Chapter 20, p 238 in Preston and Wilson (2013)
Chapter 11, p 555 in Naish and Court (2014)
Local Blood Flow (kidney)
Decreased renal blood flow
Monitored by JGA cells
Renin production
Angiotensinogen
Angiotensin I
Converting enzyme
Angiotensin II
Sodium reabsorption
Aldosterone
Potassium secretion
Vasoconstriction
Chapter 20, p 243 in Preston and Wilson (2013)
Chapter 11, p 556 in Naish and Court (2014)
Hormones
 Angiotensin II is a vasoconstrictor
 Aldosterone increases vascular sensitivity to
Angiotensin II
 ADH (anti-diuretic hormone) increases water
reabsorption
 ANF decreases sodium reabsorption
Chapter 20, p 244 in Preston and Wilson (2013)
Chapter 11, p 556 in Naish and Court (2014)
Overview
ADH
Fluid loss
Arterial pressure
Blood volume
Venous return
heart rate
vol
sympathetic
contractility
vasoconstriction
Cardiac output
baro
Arterial pressure
chemo
CNS
Cardiac output
Venous return
veins
capillary
pressure
Blood volume
Local blood flow
kidney
renin/angiotensin
aldosterone