Kidney Cortex (KC) Nitric Oxide Synthase (NOS) and Superoxide Dismutase (SOD) in Cyp1a1‐Ren2 Transgenic Rats with ANG II‐Dependent Hypertension

ANG II‐dependent hypertension (HTN) is induced in Cyp1a1‐Ren2 transgenic rats by dietary administration of 0.15% or 0.30% indole‐3‐carbinol (I3C), which produces slowly progressive and malignant HTN, respectively. Here we investigated the impact of this HTN on KC endothelial (e) and neuronal (n) NOS, and superoxide dismutase (SOD) abundance. Cyp1a1‐Ren2 rats were fed normal diet (control), a diet containing 0.15% I3C, 0.3% I3C, or 0.3% I3C+candesartan (Cand; 25 mg/L in drinking water) (n=6 per group) for 10 days. eNOS protein abundance (IOD/total protein) was increased in rats induced with both 0.15% and 0.30% I3C compared with the non‐induced controls and was prevented by the AT 1 receptor antagonist, Cand (Table, *p<0.05 vs control). In contrast, there were no changes in the abundance of nNOSα or β or any of the SOD isoforms in KC. Thus, despite other evidence that increased oxidative stress occurs in Cyp1a1‐Ren2 transgenic rats, we found no loss of SOD protein abundance in either model of HTN. The increased renal eNOS and maintained nNOS expression observed in hypertensive Cyp1a1‐Ren2 rats is consistent with functional studies which show an important role of renal NO in maintenance of renal hemodynamics in this model.