Structure and function of the arteries in hypertension.

Like tissues in other parts of the body, those of the heart and blood vessels can rapidly adapt their design. The principles of these differentiated structural changes in response to altered functional demands will be outlined in this report. With respect to arterial resistance vessels in hypertension, any sustained arterial pressure elevation leads to wall (w) hypertrophy, whereas the average inner radius (ri) decreases. The reverse occurs at sustained pressure reductions, and this process is aptly termed "structural autoregulation." By means of this structural autoregulation, wall tension per unit layer (T) remains largely constant when pressure (P) increases (decreases), according to Laplace's law: T = P X r/w. Furthermore, this structural w/ri increase, because it is a local vascular response although it is often considerably modified by neurohormonal "trophic" influences, results in a geometrically based vascular hyperreactivity affecting the systemic precapillary resistance vessels, whereas the structural ri reduction leads to an upward resetting of systemic resistance to flow which is present even at maximal vasodilation (Rmin). Because of this "structural amplifier" principle, an increased systemic resistance can be maintained even at normal vascular smooth muscle activity, and smooth muscle activations may then lead to exaggerated resistance elevations. Thus, a most important positive-feedback interaction is created between even mild functional "pressor" influences, if adequately sustained, and this normal process of structural adaptation. This positive-feedback interaction therefore gradually tends to accentuate the latter element until it entirely dominates the hemodynamics of established hypertension. As the process is induced early and established rapidly, and in primary hypertension often even seems to be genetically reinforced in various ways, it becomes of utmost pathogenetic significance. With respect to the aorta-large conduit arteries, their "Windkessel function" becomes reduced by the same process of adaptive wall thickening. This increases the pulse amplitude and thereby accentuates the systolic afterload of the left heart, the load of which is raised also because of the upward structural resetting of systemic precapillary resistance. Furthermore, the same type of structural adaptation also contributes to the upward resetting of the cardiac, arterial, and renal "barostat" mechanisms, as cardiac and arterial walls become thicker and stiffer, whereas renal preglomerular resistance vessels participate in the upward structural autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)