Fig. 1.

Basal and protein kinase C (PKC)-stimulated increases in superoxide are derived from NADPH oxidase in bovine coronary artery. Basal superoxide production in bovine coronary arteries (BCA) rings (n = 15–20) detected by lucigenin (5 μM) chemiluminescence is decreased by (A) superoxide scavengers peg-superoxide dismutase (peg-SOD; 300 U/ml), tiron (10 M), and a combination of both (A); NADPH oxidase inhibitors diphenyleneiodonium (DPI; 10 μM) and gp91^ds-tat (50 μM), but not by the xanthine oxidase inhibitor allopurinol (Allo; 100 μM) (B); and PKC inhibitors chelerythrine (Chel; 10 μM), staurosporine (Stauro; 100 nM), and calphostin C (Cal; 1 μM) (C). Conversely, superoxide generation is increased in coronary artery by cell permeable PKC activator phorbol 12,13-dibutyrate (PDBu; 10 μM), and this increase in superoxide generation is inhibited by pretreatment of coronary artery with protein kinase C inhibitors (Chel, Stauro and Cal) (D) and NADPH oxidase inhibitors (DPI and gp91^ds-tat) (E). Scrambled sequence of gp91ds-tat did not affect lucigenin chemicluminesce in basal (497 ± 69 U/mg) and PDBu (3,247 ± 201 U/mg) treated samples.