Pulsatile Stretch Induces Release of Angiotensin II and Oxidative Stress in Human Endothelial Cells: Effects of ACE Inhibition and AT1 Receptor Antagonism

Abstract

Mechanical forces and the activation of the renin-angiotensin system (RAS) may alter the NO/O₂^•− balance, imparing endothelial nitric oxide (NO) availability. This study investigates the link between RAS and NO/O₂^•− balance in human aortic endothelial cells (HAEC) exposed to pulsatile stretch with and without ACE inhibitor quinaprilat or angiotensin II type 1 (AT₁) receptor antagonist losartan. Pulsatile stretch increased Ang II levels and O₂^•− production, reducing NO release. RAS blockade with quinaprilat or losartan restored the balance between NO and O₂^•−. These results provide a molecular basis for understanding the vascular protective effects of ACE inhibition and AT₁ receptor antagonism.