Abstract
Summary: First, the multifactorial background of primary hypertension is outlined in principle, where particular attention is given to the early, sometimes even genetically reinforced structural “upward resetting” of the cardiovascular system, which soon dominates hemodynamics in both human and rat hypertension. On this basis, it is then discussed which modes of action that antihypertensive treatment could best achieve regression of the structural changes in heart and vessels. Since both the luminal and wall changes can be affected in a different manner, and since the growth processes may be reinforced by both genetic and neurohormonal “trophic” influences, there are potentially many ways by which regression could be accomplished via specific interferences, apart from the blood pressure lowering per se. As to the “hemodynamic profile” of drug interferences, reasons are given for an approach where a systemic resistance vessel dilatation is combined with a mild damping of the β-adrenergic sympathetic drive on the heart.

This publication has 0 references indexed in Scilit: