Recent advances on large arteries in hypertension.

The most classic hemodynamic concept explaining the increased mean arterial pressure in hypertension reflects an increased total peripheral resistance dynamically and an increased wall-to-lumen ratio to suppress smaller arteries. However, a more current consideration takes into account 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 constant along the arterial tree, the pulse pressure increases markedly from the more central to the peripheral arteries, indicating that in vivo each artery should be characterized according to its own blood pressure curve. This important concept implies major modifications in the methods used to investigate the relationships between mechanical factors and large artery structure and function. It therefore seems reasonable that in hypertension the large arteries should no longer be considered as passive conduits but rather in terms of their active behavioral response to the mechanical forces to which they are subjected. New investigational aspects in hypertension therefore now involve not only genetic, cellular, and molecular mechanisms but also transductional hemodynamic mechanisms reflecting changing patterns in the extracellular matrix that influence structural remodeling of the vessels.