TISSUE BLOOD FLOW
Arterioles set vascular resistance via vasoconstriction/vasodilation.
SMOOTH MUSCLE
Have gap junctions in between and act as a functional syncytium (if you get a signal
from nerve, a multiple fibres will act in sync).
Smooth muscle contraction – Ca2+ binds to calmodulin and activates myosin light
chain kinase. This causes the myosin light chain to be phosphorylated.
Phosphorylation allows cross bridge formation to occur for contraction to take
place. (Energy efficient).
Control of Blood Vessels: LOCAL or GLOBAL control.
GLOBAL CONTROL
1. Sympathetic Nervous System
With Noradrenaline acting on alpha-1 adrenoreceptors.
Sympathetic stimulation increases vasomotor tone causing vasoconstriction.
Vasoconstriction can either increase Total Peripheral Resistance which
increases afterload or can increase Central Venous Pressure which increases
preload.
2. Hormones
Hormones causing vasoconstriction (Adrenaline on alpha-1, angiotensinogen
II and Vasopressin).
Hormones causing vasodilation (Adrenaline on Beta-2, oestrogen and atrial
natriuretic peptide).
Noradrenaline and Adrenaline both increase chronotropy and inotropy. NA only acts on
alpha-1 adrenoreceptor and causes vasoconstriction.
Whereas, Adrenaline gives a mixed effect of vasoconstriction at alpha-1 adrenoreceptor
(increased heart rate) and vasodilation at Beta-2 adrenoreceptor (increase oxygen supply).
Use Adrenaline in Local Anaesthetics – causes vasoconstriction to reduce bleeding and also
helps to retain the anaesthetic in the region where it has been inserted; therefore,
increasing anaesthetic efficacy.
Vasopressin – also known as anti-diuretic hormone, initiated in response to low blood
volume, prevents you from urinating to increase fluid. Vasopressin is released from posterior
pituitary to cause vasoconstriction; however, fortunately it doesn’t vasoconstrict cerebral or
coronary vessels.
RAAS System – Stimulus for Renin-Angiotensin-Aldosterone System is low blood volume;
therefore, renin release activates angiotensin I. Angiotensin I is converted into Angiotensin II
which can cause aldosterone release to increase water retention and increase preload.
LOCAL CONTROL
1. Autocoids
Chemicals produced locally and act locally regulating blood flow.
Arterioles set vascular resistance via vasoconstriction/vasodilation.
SMOOTH MUSCLE
Have gap junctions in between and act as a functional syncytium (if you get a signal
from nerve, a multiple fibres will act in sync).
Smooth muscle contraction – Ca2+ binds to calmodulin and activates myosin light
chain kinase. This causes the myosin light chain to be phosphorylated.
Phosphorylation allows cross bridge formation to occur for contraction to take
place. (Energy efficient).
Control of Blood Vessels: LOCAL or GLOBAL control.
GLOBAL CONTROL
1. Sympathetic Nervous System
With Noradrenaline acting on alpha-1 adrenoreceptors.
Sympathetic stimulation increases vasomotor tone causing vasoconstriction.
Vasoconstriction can either increase Total Peripheral Resistance which
increases afterload or can increase Central Venous Pressure which increases
preload.
2. Hormones
Hormones causing vasoconstriction (Adrenaline on alpha-1, angiotensinogen
II and Vasopressin).
Hormones causing vasodilation (Adrenaline on Beta-2, oestrogen and atrial
natriuretic peptide).
Noradrenaline and Adrenaline both increase chronotropy and inotropy. NA only acts on
alpha-1 adrenoreceptor and causes vasoconstriction.
Whereas, Adrenaline gives a mixed effect of vasoconstriction at alpha-1 adrenoreceptor
(increased heart rate) and vasodilation at Beta-2 adrenoreceptor (increase oxygen supply).
Use Adrenaline in Local Anaesthetics – causes vasoconstriction to reduce bleeding and also
helps to retain the anaesthetic in the region where it has been inserted; therefore,
increasing anaesthetic efficacy.
Vasopressin – also known as anti-diuretic hormone, initiated in response to low blood
volume, prevents you from urinating to increase fluid. Vasopressin is released from posterior
pituitary to cause vasoconstriction; however, fortunately it doesn’t vasoconstrict cerebral or
coronary vessels.
RAAS System – Stimulus for Renin-Angiotensin-Aldosterone System is low blood volume;
therefore, renin release activates angiotensin I. Angiotensin I is converted into Angiotensin II
which can cause aldosterone release to increase water retention and increase preload.
LOCAL CONTROL
1. Autocoids
Chemicals produced locally and act locally regulating blood flow.
