Effects of ACE inhibition on circulating endothelial progenitor cells, vascular damage, and oxidative stress in hypertensive patients

Abstract

Purpose: The pathogenic role of ACE inhibition in hypertensive patients regarding to endothelial progenitor cell (EPC) function is still poorly understood. The aim of the study was to evaluate both EPC number and function and their relationship to carotid intimal medial thickness (IMT) progression. Methods:We studied 36 newly diagnosed mildly hypertensive patients free of cardiovascular disease and related risk factors without prior or concurrent therapy with ACE inhibitors. Patients were randomized to receive enalapril 20 mg/die (n=18) or zofenopril 30 mg/die (n=18). EPC number and migrating capacity, plasma nitrite/nitrate (NOx) and isoprostane concentrations were evaluated. Carotid intimal media thickness (IMT) was determined by ultrasonography at baseline and after 1 and 5 year follow-up.Results: EPC number increased during the follow-up with no statistical differences between treatment groups. There was an inverse correlation between circulating EPCs and IMT increase over the time. Plasma nitrite/nitrate decreased during the study without evident differences between the treatment groups. Isoprostanes decreased more markedly in zofenopril treated patients. Multiple linear regression model demonstrated that the carotid IMT was significantly inversely correlated with EPC but not with migratory cells after adjustment for confounders. Conclusions:The present study demonstrated that EPC levels increased during the follow-up in both groups of newly diagnosed hypertensive patients treated with ACE-inhibitors. These drugs prevented the progression of vascular damage with an inverse correlation between circulating EPC levels and IMT values.4

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“…There is conflicting evidence to suggest that ACEi/ARBs can alter the bioavailability of NOx with some studies showing reduction [40] and others proposing increases [41,42]. Therefore the direction in which ACEi/ARBs may alter the bioavailability of NO remains unclear.…”

Challenges in hypotensive therapy: the role of calcium antagonists

“…Кроме того, лер-канидипин обнаружил способность снижать актив-ность матриксных металлопротеаз, индуцированной NO-синтазы и фактора некроза опухоли альфа. Это имеет прямое отношение к предотвращению ослож-нений атеросклероза, снижению активности воспа-ления в стенке сосуда, улучшению функции эндоте-лия [4,5]. Следует отметить, что современная терапия артериальной гипертонии не может ограничиваться только снижением давления.…”

Arterial hypertension treatment with a calcium channel blocker and an ACE inhibitor. Benefits of combination therapy

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