'Structural autoregulation'--the local adaptation of vascular beds to chronic changes in pressure.

Blood vessels readily adapt their design in response to sustained functional changes. If pressure (P) increases, the resulting thickening of the walls (w) of the resistance vessels, associated with a reduction in average inner radius (ri), keeps wall tension per unit wall layer (T) constant, because the increased w/ri ratio largely balances the raised pressure (Laplace's law: T = P X ri/w). The opposite occurs when there are sustained reductions in pressure. This locally elicited, mainly precapillary structural adaptation is a long-range equivalent to precapillary functional autoregulation and deserves to be called structural autoregulation. In primary hypertension there is an early 'structural resetting' of the systemic precapillary resistance, due to narrowing of ri and to vascular hyperreactivity ensuing from the increase in w/ri. These structural changes imply an increased resistance to flow at normal levels of vascular smooth muscle activity. Furthermore, even mild functional pressor influences will, if sustained, by a positive feedback interaction with the initially mild vascular hyperreactivity gradually accentuate the structural increase in w/ri. Marked rises in pressure may ensue from this interaction, implying that it is a major causative element in primary hypertension. As the renal preglomerular resistance vessels are similarly structurally autoregulated, this implies an early largely parallel resetting of the important renal 'long-term barostat function'. Further, as the walls of large arteries get thicker and stiffer, this helps to reset the baroreceptors. Finally, as the venous capacitance vessels adapt in a similar way the slight rise in average venous pressure in primary hypertension will reduce venous compliance, which helps to 'centralize' the usually slightly reduced blood volume.