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Arterial acceleration
The theory of arterial acceleration proposes that the pressure wave from the heart is enhanced by a short-lasting contraction of the smooth muscle cells in the wall of conducting arteries. At stroke onset the sudden rise in pressure is expected to cause a stretch induced depolarisation within the smooth muscle cells of the aorta: the myogenic response. Via gap junctions, abundantly available in smooth muscle cells, this depolarisation wave spreads along the arterial tree. Depolarisation of smooth muscle cells is followed by Calcium influx resulting in contraction. In this way the arterial tree stiffens during the early phases of systole. A peristaltic wave occurs that transmits the pressure wave resulting from early heart contraction along the branches of the arterial tree into even the most remote capillary networks. This contraction is assumed short-lasting, only active during the first 100-150 ms of systole as not to oppose the actual ejection phase of the heart.

The theory of arterial acceleration explains why, despite the increase in overall cross-sectional area, the pulse pressure is not diluted along its way down the arterial tree. It also explains why the pulse pressure reaches all capillary systems within the body not only favouring tissues closest to the heart.

The theory of arterial acceleration is an alternative to the theory of arterial stiffness. Both theories aim to explain the biphasic appearance of the systolic phase of a recording of pressure or flow within the arteries. The theory of arterial stiffness assumes that the flow within an artery at any moment in time depends upon a forward travelling pressure wave from the heart and backward travelling waves from points of high resistance in the periphery. Thereby, the theory of arterial stiffness assumes that the energy of heart contraction is opposed by the periphery: the pressure becomes higher but the flow becomes lower during the second phase of systole. The theory of arterial acceleration, in contrast, proposes that the energy of heart contraction is enhanced by the temporary contraction within the conducting arteries: the pressure and the flow become higher during the first phase of systole.

Application
At present there is no convincing evidence favouring one of both theories. Both theories are tested empirically in pathophysiological studies of, for instance, end stage renal failure, hypertension, diabetes mellitus or  sepsis.