Angiotensin II receptor blocker attenuates overexpression of vascular endothelial growth factor in diabetic podocytes.

摘要: VEGF expressed in glomerular podocytes, is known to increase vascular permeability macromolecules. Angiotensin II can stimulate the release of VEGF, and protective effects angiotensin antagonist against diabetic injury suggest that II-induced an important pathogenetic mechanism development proteinuria during nephropathy although this not fully understood. In study, changes expression was examined experimental determine whether these were modified by renoprotective intervention blockers receptors. The streptozotocin- induced rats treated with L-158,809, a blocker receptors, for 12 weeks. Age-matched L-158,809 served as controls. RT-PCR immunohistochemistry used assess quantify gene protein VEGF. A progressive urinary excretion observed rats. Glomerular significantly higher than control groups, significant reduction L-158,809- mRNA also kidneys L-158,809-treated kidneys. These results demonstrates increased receptor attenuated prevented vivo. Attenuation podocytes could contribute antagonists nephropathy.