Renal autoregulation is not impaired during early streptozotocin diabetes mellitus (DM) in Long‐Evans rats

Abstract

Diabetes is a leading cause of chronic kidney disease and increases susceptibility to blood pressure induced glomerular injury. Autoregulation is the only mechanism that protects the glomeruli when blood pressure fluctuates. Impaired autoregulation has been reported in early DM and attributed to increased nitric oxide (NO) but intact autoregulation has been demonstrated in established DM. We hypothesized that intrarenal NO increases in early DM with corresponding impairment of autoregulation and that neuronal NOS (nNOS) contributes to the increased NO. Male Long‐Evans rats were divided into two groups: one week diabetic (N=5) and one week intact (N=3). Diabetes was induced with streptozotocin (60mg/kg i.v.) and depot insulin was used to keep blood glucose ~20–24 mmol/L. Rats were anaesthetized (isoflurane) and their left kidneys were exposed. Renal perfusion pressure was forced with a servo‐controlled aortic occluder and the resulting renal blood flow was measured with an ultrasound flow probe during control, nNOS inhibition (L‐VNIO) and non selective NOS inhibition (L‐NAME). Renal autoregulation was intact in all animals except one intact animal. nNOS protein distribution was similar and was little response to either NOS inhibitor in all rats. We conclude that renal autoregulation is not impaired, and that intrarenal NO does not play a role in early diabetes in these rats. Supported by CIHR MOP‐102694.