Large arteries and angiotensin II blockade in hypertension

Renin-angiotensin blockade has reduced cardiovascular morbidity and mortality in hypertensive subjects. Experimental studies have shown that this blockade acts primarily on vascular tone, causing quasi simultaneously a decrease in vascular resistance, an increase in large artery compliance and a change in endothelial function independent of blood pressure changes. In hypertensive models, the reduction of arterial hypertensive hypertrophy is proportional to blood pressure reduction while the reduction of collagen is responsible for the elasticity improvement and only dependent on angiotensin II. Molecular biology shows that, under the control of MAP-kinase, the major substratum of the action is the biochemical complex between the integrin alpha5 beta1 and its ligand fibronectin, both highly sensitive to mechanical pulsatility and effects on collagen fibers. Following the Reason study, numerous therapeutic trials in hypertension have shown not only the antihypertensive effect of this complex but also its impact on pulsatility and finally on central systolic and pulse pressure.