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

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.

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.

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).

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.