Endothelial nitric oxide synthase (eNOS) deficiency may contribute to the pathogenesis of
diabetic nephropathy in both experimental models and humans, but the underlying
mechanism is not fully understood. Here, we studied two common sequelae of endothelial
dysfunction in diabetes: glomerular capillary growth and effects on neighboring podocytes.
Streptozotocin-induced diabetes increased glomerular capillary volume in both C57BL/6
and eNOS−/− mice. Inhibiting the vascular endothelial growth factor receptor attenuated …