The theory of arterial stiffness explains why blood pressure profiles and blood flow velocity profiles change as they do along the branching arterial tree. Blood expelled from the heart into the aorta during systole shows a parabolic profile over time. Nevertheless, when we measure blood velocities more downstream, the profile of the blood flow velocity turns into a more biphasic signal.

The theory of arterial stiffness  proposes that these profile changes occur due to recurrent waves. The positive pressure wave from the heart reflects against the high resistance of peripheral arteries. At every location in the arterial tree the pressure measured is a combination of the forward traveling wave from heart contraction and backward traveling waves from different points of reflection. Thus, the reflecting waves form an obstacle to the blood flow and energy of cardiac contraction is lost.

The theory of arterial acceleration proposes that energy is added to the pressure wave from the heart. The increase in aortic pressure at stroke onset triggers the myogenic response in smooth muscle cells. This stretch induced depolarisation spreads rapidly via gap junctions between individual cells. Thereby a wave of depolarisation sweeps along the arterial tree from proximal to distal and into the most remote capillary systems. The depolarisation triggers calcium influx resulting in a short lasting contraction of the smooth muscle cells.

In this way arterial acceleration augments the pressure wave from the heart traveling at high speed as a peristaltic wave along the arterial tree. Since it is at stroke onset and only short-lasting it does not interfere with the ejection phase of the heart. The arterial acceleration allows the pressure generated during the first instances of myocardial contraction to spread along all branches of the arterial tree and enter into even the most remote capillary systems.

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