The aortic biochemical properties are reported to be altered in stroke-prone spontaneously hypertensive rats (SHR-SPs) as a result not only of the accelerated accumulation of advanced glycation end products (AGEs) in thoracic aortae but also of primary defects. There is a growing body of evidence that reactive oxygen species (ROS) are involved in the formation of AGEs. We propose here a novel hypothesis that SHR-SPs are the strain that genetically produce more ROS generations. Since ROS formations and AGE accumulations play central roles in the pathogenesis of diabetic microvascular complications, SHR-SPs might be more susceptible to vascular complications when induced to be diabetic. To reveal new genes involved in susceptibility to diabetic microangiopathies through the study of these animal models might be a valuable strategy to develop novel therapeutic approaches.
Copyright 2001 Harcourt Publishers Ltd.