Structural factors: the vascular wall. Consequences of treatment.

Abstract

Like all tissues, blood vessels readily adapt their structure upon sustained functional changes. For example, pressure increases soon induce a largely proportional wall (w) thickening, where arteries, veins, and true resistance vessels respond alike. The latter also show a modest structural narrowing of average inner radius (ri), where the increased w/ri ratio results in a geometrically based vascular hyperreactivity. In primary hypertension, this type of precapillary resistance vessel adaptation implies an important "upward structural autoregulation" of systemic resistance, which is thereby kept increased also when vascular smooth muscle activity is entirely normal. Further, the systemic vascular hyperreactivity introduces a positive feedback interaction with functional pressor influences. By this mechanism, even marginal increases in "functional drive" may, if only sustained, steadily enhance the structural w/ri increase until it dominates hemodynamics. Similar alterations of the renal preglomerular vessels cause an early upward resetting of the renal barostat function, while wall thickening of large arteries helps to reset the baroreflexes. Also, the capacitance vessels show some structural adaptation that reduces venous compliance and contributes to blood volume centralization. Due to this overall structural resetting of hypertensive cardiovascular systems, the pharmacological problem of normalizing blood pressure is not one of merely damping an increased vascular smooth muscle activity. The task is more formidable, because effector cell activity must be kept even subnormal, despite counterregulatory mechanisms. These mechanisms almost all have been redesigned to maintain the high pressure state, with the long-range goal that true regression toward normality should ultimately ensue.