Vascular changes in hypertension. Therapeutic implications.

Abstract

A review of the general nature of cardiovascular structural adaptation and how this per se normal process becomes of key haemodynamic importance for the development of primary hypertension, particularly with respect to the gradual elevation of systemic precapillary resistance is presented. Because of the structural 'upward resetting' of the haemodynamic equilibrium, antihypertensive therapy in reality faces a far more formidable task in chronic hypertension than merely 'normalising' a supposedly raised vascular smooth muscle activity or/and cardiac output. Rather, it must bring about sub-normal activity levels to normalise the arterial pressure level, and only when such a pressure lowering has been sustained enough to allow for structural regression towards normal dimensions is a true normalisation achieved. However, the process of structural regression takes time and is complicated by the fact that the often long duration of the high-pressure state has led to structural changes which can be quite difficult to reverse. Finally, physiological-haemodynamic reasons are discussed which direct pharmacological interferences preferentially towards the pronounced myogenic activity of the precapillary resistance vessels, which both in normo- and hypertension is by far the most dominating element behind resting smooth muscle activity in these vessels and is, moreover, especially dependent on influx of external calcium ions. As the raised precapillary resistance (by means of 'structural autoregulation') represents the key element behind the pressure rise in established hypertension, such a pharmacological interference is directed towards the proper haemodynamic site and would not directly interfere with the neurohormonal integrative control of the circulation.