Effects of the angiotensin-converting enzyme (ACE) inhibitor perindopril on endothelial and platelet functions in essential hypertension

Endothelial damage and platelet hyperactivity may play a role in the vascular complications of essential hypertension. Restoration of endothelial function and reduction of increased platelet aggregation in essential hypertension are one of the aims of modern anti-hypertensive therapy. Therefore, the effect of angiotensin converting enzyme (ACE) inhibitors on endothelial and platelet functions is of interest. In the present study, 23 healthy normotensives and 23 age- and sex-matched patients with non-treated essential hypertension (1st and 2nd stage according to WHO) were investigated. Measurements of endothelial and platelet functions in hypertensives were carried out before therapy, after 1 week of placebo administration, after 1 week and after 1 month of perindopril therapy in a once daily dose of 4 mg. Plasma thrombomodulin (ELISA method) and beta-thromboglobulin (radio immunoassay method) were assayed and platelet aggregation (spontaneous and induced by adrenaline) was measured. The values of plasma thrombomodulin, a novel marker of endothelial function, were compared between age- and sex-matched normotensives and hypertensives. A significant decrease of adrenaline-induced platelet aggregation was observed after 1 month of perindopril therapy in comparison with the values before therapy or after 1 week of perindopril therapy ( P < 0.02 and P < 0.05 respectively). There were no significant changes in plasma thrombomodulin or beta-thromboglobulin following therapy. We failed to find significant changes of plasma thrombomodulin in patients in the early stages of hypertension, but its tendency to be higher than in normotensives does not rule out some vascular damage. The inhibitory effect of perindopril on platelet aggregation may be a further advantage of this drug. Since no changes were found after 1 week of therapy, the reduction of adrenaline-induced platelet aggregation after 1 month of therapy may be explained by an indirect effect of perindopril on platelet function, probably asa result of protective action on the arterial wall.