Fig. 5.
Production of NOx from L-NAME in vivo and in cells, and its relation to nitrodilator-mediated vasodilation. A) Experimental protocol for measurements of 15N and 14N+15N NOx levels in rats. B-D)15N and 14N+15N NOx levels in B) plasma, and homogenates of C) various tissues and D) mesenteric and femoral arteries (n=4). E) ROS levels in RAW264.7 macrophages that had been incubated in the presence and absence of hypoxia, Antimycin A, deferoxamine, or resveratrol. One-way ANOVA, n=3. F) NOx levels in lysates of cells that had been incubated with or without L-NAME (1 mmol/L) under conditions of (E). NOx levels in cell lysates were measured by triiodide-based chemiluminescence. White columns in (F) show values for NOx production from L-NAME. One-way ANOVA, n=3. G) ROS levels in macrophages incubated in the presence and absence of catalase (n=3). H) NOx levels in cell lysates and changes with incubation. One-way ANOVA with Tukey's test for left four columns; t test for right two columns. I-J) Co-administration of catalase (16.5 mg·kg-1·day-1; i.p.; 4 days) augments the potentiation effects of prior L-NAME treatment on I) NTG (n=5-6) and J) GSNO (n=3) mediated vasodilation. Note the null effects of L-NMMA + catalase. Two-way ANOVA. K) Proposed schema for the relation between L-NAME's NO contributing property and subsequent nitrodilator-mediated vasodilation. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 vs. Control.