The most classic hemodynamic concept explaining the increased mean art
erial pressure in hypertension reflects an increased total peripheral
resistance dynamically and an increased wall-to-lumen ratio to suppres
s smaller arteries. However, a more current consideration takes into a
ccount not only that steady component but also the pulsatile component
of blood pressure, a point that importantly modifies the traditional
hemodynamic definition. Whereas mean arterial pressure is almost const
ant along the arterial tree, the pulse pressure increases markedly fro
m the more central to the peripheral arteries, indicating that in vivo
each artery should be characterized according to its own blood pressu
re curve. This important concept implies major modifications in the me
thods used to investigate the relationships between mechanical factors
and large artery structure and function. It therefore seems reasonabl
e that in hypertension the large arteries should no longer be consider
ed as passive conduits but rather in terms of their active behavioral
response to the mechanical forces to which they are subjected. New inv
estigational aspects in hypertension therefore now involve not only ge
neric, cellular, and molecular mechanisms but also transductional hemo
dynamic mechanisms reflecting changing patterns in the extracellular m
atrix that influence structural remodeling of the vessels.