[Effect of cilazapril, a converting enzyme inhibitor, on cardiovascular hypertrophy in the hypertensive patient].

The sustained increase in peripheral vascular resistance is the hemodynamic alteration characteristic of the established adult hypertension. This is the result of a vascular tone increase and/or structural changes which imply hypertrophy as well as hyperplasia of the vascular smooth muscle fibers, hypertrophy of the cardiac cells and an increase in the constituent synthesis of the extracellular matrix. Angiotensin II and noradrenalin exert major trophic effects which accelerate the progression of cardiovascular hypertrophy being the cardiovascular system very sensitive to the trophic actions of renin-angiotensin. Angiotensin II induces the expression of the A-chain of the growth factor of platelet origin, of the baseline fibroblastic growth factor and of the B-transformer factor and, moreover, stimulates type I and type III collagen synthesis and favors trophic factors release. Therefore, the renin-angiotensin system plays an important role in growth regulation and myocyte remodelation and in the cardiovascular extracellular matrix which is mediated through specific receptors, since it can be inhibited by ATI receptor antagonists for angiotensin II and ACE. Cilazapril is an ACE long duration agent which produces a reduction of both blood pressure and cardiovascular hypertrophy. This is a multiple action mechanism exerting a vasodilator action, inhibiting the sympathetic tone or increasing kinine levels and inhibiting the cardiac and vascular renin-angiotensin system.