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From the Department of Internal Medicine and INSERM (U337), Broussais
Hospital, Paris (M.E.S., R.A.), and Manhès Center, Fleury Merogis
(G.M.L.), France; and Alton Ochsner Medical Foundation, New Orleans, La
(E.D.F.).
Correspondence to Professeur Michel Safar, Médecine Interne 1, Hôpital Broussais, 96 rue Didot, 75674, Paris, Cedex 14, France.
Abstract
Abstract—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.
© 1998 American Heart Association, Inc.
Third Workshop on Structure and Function of Large Arteries: Part I
Recent Advances on Large Arteries in Hypertension
Key Words: hemodynamics • transduction • arteries • vessels • vascular remodeling
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