Abstract
Cardiovascular complications are preceded by endothelial dysfunction in type 2 diabetes. This is associated with increased plasma reactive oxygen species (ROS). High ROS levels reduce nitric oxide bioavailability and attenuate vasodilation. The ACE inhibitor ramipril is frequently used in managing the cardiovascular complications of diabetes. We hypothesized that ramipril treatment improves ACh‐induced, endothelium‐dependent vasodilation in db/db mice. We treated 5‐week‐old wild‐type (WT) and type 2 diabetic (db/db) mice with vehicle or ramipril (10mg/kg/day) for 6 weeks. Plasma ROS levels were reduced by ramipril in WT (34%) and db/db (51%) mice. Ramipril treatment increased ACh‐induced vasodilation by 4‐fold in db/db mice without affecting endothelium‐independent vasodilation. These data support a key role for angiotensin II in mediating endothelial dysfunction in diabetes through the generation of ROS. (Supported by Heart and Stroke Foundation of Canada & Singapore Ministry of Education Academic Research Fund)
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