Treatment of arterial hypertension is an important part of the medical care provided in industrialized countries today. Its rationale comes from large-scale intervention trials which have shown that lowering of elevated blood pressure reduces cardiovascular morbidity and mortality. Nevertheless, during the last few years it has been shown that treated hypertensive patients are still at an increased risk of cardiovascular morbidity and mortality compared with untreated normotensive subjects of the same age and sex. Possible explanations for this disappointing finding are that blood pressure has not been lowered to strictly normotensive levels; that some elements of the excess morbidity and mortality are not prevented by antihypertensive therapy, e.g., the part attributable to coronary artery disease; or that the drugs used may themselves have negative effects, e.g., on serum lipids, which may offset the positive effects of lowered blood pressure. It is desirable that antihypertensive treatment produces a reversal of hypertension-induced structural cardiovascular changes such as left ventricular hypertrophy or increased wall/lumen ratio in the precapillary blood vessels, but many of the current antihypertensive drug regimens have no effect on structural cardiovascular changes. Against this background it would appear logical to make renewed efforts to reduce blood pressure into the clearly normotensive range in an attempt to lower the excess risk demonstrable in treated hypertensive patients. It would also seem logical to use antihypertensive drugs that could also be expected to have positive effects on hypertension-induced structural cardiovascular changes.(ABSTRACT TRUNCATED AT 250 WORDS)