Histochemical assessment of nitric oxide synthase activity in aortic endothelial cells of streptozotocin-induced diabetic rats M Shafiei, M Nobakht, M Fattahi, L Kohneh-Shahri, M Mahmoudian Pathophysiology Volume 10, Issue 1, Pages 63-67 (December 2003) DOI: 10.1016/j.pathophys.2003.08.001
Fig. 1 Concentration-dependent relaxation to the endothelium-dependent vasodilator acetylcholine in control (n=8) and diabetic (n=8) aortic rings precontracted with submaximal concentrations of phenylephrine. Values are expressed as the mean±S.E.M. (*P<0.01). Pathophysiology 2003 10, 63-67DOI: (10.1016/j.pathophys.2003.08.001)
Fig. 2 Concentration-dependent relaxation to isosorbide dinitrate in control and diabetic aortic rings with endothelium ((a), n=8) or without endothelium ((b), n=8) precontracted with submaximal concentrations of phenylephrine. Values are expressed as the mean±S.E.M. Pathophysiology 2003 10, 63-67DOI: (10.1016/j.pathophys.2003.08.001)
Fig. 3 Light micrograph of aorta obtained from healthy rat. No staining could be detected in control sections after omitting βNADP in NADPH-diaphorase staining. Pathophysiology 2003 10, 63-67DOI: (10.1016/j.pathophys.2003.08.001)
Fig. 4 Light micrograph of aorta obtained from healthy rat. NADPH-diaphorase histochemistry reveals eNOS activity in endothelial cells that strongly are stained. Pathophysiology 2003 10, 63-67DOI: (10.1016/j.pathophys.2003.08.001)
Fig. 5 Light micrograph of aorta obtained from diabetic rat. Endothelial cells show much less staining for NADPH-diaphorase. Arrows point to the sites of disruption in endothelial cell membranes. Pathophysiology 2003 10, 63-67DOI: (10.1016/j.pathophys.2003.08.001)