Hypertensive structural changes in systemic precapillary resistance vessels: how important are they for in vivo...

To discuss recent findings that seem to question the importance of structural vascular changes for the raised resistance observed in hypertension.

First, in daily life situations, the proximal resistance sections, which are the main site for vasoconstrictor fibre effects, are also the main site for structural elevation of resistance in hypertension. The most distal ones are crucially important for local flow distribution, and their unaltered design suggests that they are usually protected from pressure elevations by a raised resistance upstream. Furthermore, recent findings indicate that central neurohormonal mechanisms are much more important than myogenic ones for inducing hypertension at least in spontaneously hypertensive rats. Second, the function of structurally altered resistance vessels is often misunderstood, mainly because the haemodynamic importance of wall distensibility is disregarded. Vascular geometric design and distensibility tend to be altered to an 'ideal' extent, so that with ordinary changes in smooth muscle activity a normal flow range is maintained, despite elevations in both perfusion and transmural pressures and in resistance. Third, the rapid normalization of blood pressure on declipping of two-kidney, one clip or of one-kidney, one clip renally hypertensive rats by no means refutes the haemodynamic importance of a prevailing structural upward resetting. Declipping leads to a powerful and prolonged release of vasodilator-sympathoinhibitory medullipins, which create a subnormal smooth muscle tone. Because the structurally hyper-reactive resistance vessels now operate along a steeper resistance curve the pressure fall becomes, if anything, accentuated, which opens the way for structural regression. Fourth, the highly sophisticated and often differentiated neurohormonal control system usually explains why vasoactive agents, for example, do not regularly produce exaggerated pressure changes in vivo, even in the presence of hypertensive structural changes. In addition, counteracting effects by endothelial mechanosensitive mechanisms seem to be of great importance in these situations.

The arguments and views outlined recently do not, on closer scrutiny and for the reasons given, really challenge the importance of structural vascular changes in hypertension in vivo and may, indeed, in some respects serve to support this concept.