The effect of angiotensin-converting enzyme inhibition on inflammatory and angiogenic factors in hypercholesterolemia

Background renin-angiotensin system (ras) can be activated during hyperlipidemia. angiotensin ii increases the migration of monocytes,cytokine levels,and gene expressions of vegf and vcam-1. with this in mind,the present work attempted to investigate the effect of angiotensin-converting enzyme (ace) inhibition on vegf,vcam-1,and nitric oxide (no) serum levels in hypercholesterolemic rats. methods forty male wistar rats were divided into 4 groups including normal diet + saline injection (control),hypercholesterol diet + saline injection,normal diet + captopril injection,and hypercholesterol diet + captopril injection. before and after the beginning of the diet and after the treatment,the serum levels of cholesterol,triglycerides,ldl,hdl,and no were measured. finally,gene expressions of vcam-1 and vegf in the vascular cells from aorta were determined. results hypercholesterolemic diet increased the serum levels of cholesterol,ldl (p < 0.001),triglycerides (p < 0.01) and decreased hdl (p < 0.001). captopril caused a reduction in the serum levels of cholesterol,ldl (p < 0.001),and triglycerides (p < 0.05) as well as an increase in hdl levels (p < 0.01). although the serum levels of no decreased after hypercholesterolemic diet (p < 0.001),no significant change was observed after the treatment. increased gene expressions of vegf (p < 0.05) and vcam-1 (p < 0.01) in hypercholesterolemia were regressed in captopril treated rats (p < 0.01 and p < 0.05,respectively). conclusion captopril,an ace inhibitor,improves hyperlipidemia and prevents from overexpression of genes for vegf and vcam-1,that are implicated in the inflammation and angiogenesis. © 2015 institute of pharmacology,polish academy of sciences. published by elsevier sp. z o.o. all rights reserved.