16 Mechanism and Consequence of Vasomotion
263
depolarizes towards 0 mV Ca
2+ selective channels open and Ca
2+ runs into the cell
down its electrochemical gradient. The resulting intracellular increase Ca
2+ concentration activates contractile proteins and the smooth muscle cell contract. When the
cell membrane repolarizes the Ca
2+ channels closes and Ca
2+ is pumped out of the
cell. Importantly the smooth muscle cells (and also the endothelial cells) constitute
an electrical syncytium because they are connected by low resistance channels (gap
junctions), allowing current to flow from one cell to the next. When the cells are
activated by vasoconstrictors e.g. noradrenaline from nerves in the vessel wall, Ca
2+
is also released from stores inside the cells, which adds to the Ca
2+ increase induced
by depolarization of the membrane. The sensitivity of the contractile proteins to Ca
2+
can be modified through a number of relatively complex biochemical pathways.
16.2 The Concept of Vasomotion
The tone of the vascular smooth muscle cells often oscillate. This leads to the
phenomenon of vasomotion which is a cyclic variation in vessel diameter. Vasomotion is present in most, if not all, small arteries in both animals and humans. The
first description of vasomotion was in bat wing veins [31], i.e. the blood vessels
which leads from the tissues to the heart. Vasomotion of veins is a well studied
phenomenon [59]. Vasomotion leads to flowmotion, where the flow into a tissue or a
whole organ oscillates. Flowmotion can be seen in the intact animal or human where
it can be divided and characterized within five or six different frequency bands [33,
34, 54]—from 0.008 Hz to 1–2 Hz—associated with different aspects of the vascular
function (e.g. endothelium dependent, nerve dependent, smooth muscle dependent
etc.). Vasomotion also occurs when an artery is removed from the body and suspended
in an organ bath [16, 43], demonstrating that vasomotion is an inherent property of
the vascular wall. The prevalence of vasomotion varies between different vascular
beds, between blood vessel branching orders, and between arteries and veins and
is changed in many pathological conditions e.g. hypertension [42, 47], diabetes [4],
ischemia [49] and Alzheimer’s disease [10]. Vasomotion appears to disappear in
elderly people and yet, as it will be seen, we still do not fully understand what the
consequences of vasomotion are.
16.3 How Does Vasomotion Develop?
For vasomotion to occur there is a requirement for an oscillator and for a mean
of synchronizing the oscillations in the many smooth muscle cells in the arterial
wall. There is undoubtedly a number of ways in which this can be achieved. There
is, however also some mechanisms which very likely are important for most types
of vasomotion. It seems likely that there is no single pacemaker cell or group of
pacemaker cells which sets up the oscillation. Rather, there is evidence that at least
263
depolarizes towards 0 mV Ca
2+ selective channels open and Ca
2+ runs into the cell
down its electrochemical gradient. The resulting intracellular increase Ca
2+ concentration activates contractile proteins and the smooth muscle cell contract. When the
cell membrane repolarizes the Ca
2+ channels closes and Ca
2+ is pumped out of the
cell. Importantly the smooth muscle cells (and also the endothelial cells) constitute
an electrical syncytium because they are connected by low resistance channels (gap
junctions), allowing current to flow from one cell to the next. When the cells are
activated by vasoconstrictors e.g. noradrenaline from nerves in the vessel wall, Ca
2+
is also released from stores inside the cells, which adds to the Ca
2+ increase induced
by depolarization of the membrane. The sensitivity of the contractile proteins to Ca
2+
can be modified through a number of relatively complex biochemical pathways.
16.2 The Concept of Vasomotion
The tone of the vascular smooth muscle cells often oscillate. This leads to the
phenomenon of vasomotion which is a cyclic variation in vessel diameter. Vasomotion is present in most, if not all, small arteries in both animals and humans. The
first description of vasomotion was in bat wing veins [31], i.e. the blood vessels
which leads from the tissues to the heart. Vasomotion of veins is a well studied
phenomenon [59]. Vasomotion leads to flowmotion, where the flow into a tissue or a
whole organ oscillates. Flowmotion can be seen in the intact animal or human where
it can be divided and characterized within five or six different frequency bands [33,
34, 54]—from 0.008 Hz to 1–2 Hz—associated with different aspects of the vascular
function (e.g. endothelium dependent, nerve dependent, smooth muscle dependent
etc.). Vasomotion also occurs when an artery is removed from the body and suspended
in an organ bath [16, 43], demonstrating that vasomotion is an inherent property of
the vascular wall. The prevalence of vasomotion varies between different vascular
beds, between blood vessel branching orders, and between arteries and veins and
is changed in many pathological conditions e.g. hypertension [42, 47], diabetes [4],
ischemia [49] and Alzheimer’s disease [10]. Vasomotion appears to disappear in
elderly people and yet, as it will be seen, we still do not fully understand what the
consequences of vasomotion are.
16.3 How Does Vasomotion Develop?
For vasomotion to occur there is a requirement for an oscillator and for a mean
of synchronizing the oscillations in the many smooth muscle cells in the arterial
wall. There is undoubtedly a number of ways in which this can be achieved. There
is, however also some mechanisms which very likely are important for most types
of vasomotion. It seems likely that there is no single pacemaker cell or group of
pacemaker cells which sets up the oscillation. Rather, there is evidence that at least